Not good news on the research front.

A study published Monday in the journal Pediatrics indicates about 1% of children 3 to 17 have autism or related disorder

Results based on national telephone survey of more than 78,000 parents
CDC official: “This is a significant issue that needs immediate attention”
Researchers saying finding could reflect heightened awareness of disorder

Today, 1 in 91 have Autism.  Boys were four times as likely as girls to have ASD, and non-Hispanic black and multiracial children were less likely than non-Hispanic white children.

The question on everyone’s ,mind is where will these children go to school and what will become of their lives as they enter adulthood.

The Educational system and job market is already overburdened. We need to act quickly on all fronts, Quickly with intervention, quickly with therapy and services and in providing a better Education opportunity.

Now I must go and update my User Name to 1 in 91, down form 1 in 150 children have Autsim today.

PS – I am not liking what I am hearing about candles recently. Cheap candles are horrible to burn inside. The wick may contain lead and the wax is filled with nasty stuff… So many things correlate with the rise in ASD- computers and the web, cellphones, plastic bottles, Korean cars it could be anything and everything…

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With autism, parents have extreme concerns about future independence, finances and isolation, compared to more common worries of parents with typically developing children

(Washington, December 16, 2008) — Parents of children with autism are struggling with a host of worries that impact every aspect of their lives, and are particularly fearful that their family will lack the life-long supports needed to address the significant challenges of autism, according to a new study released today by Easter Seals and made possible by MassMutual Financial Group.

Easter Seals’ Living with Autism Study results reveal parents raising children with autism are very concerned about the future independence of their children. In fact, they’re far more concerned than parents of typically developing children — nearly 80 percent say they’re extremely or very concerned about their children’s independence as an adult, compared to only 32 percent of other parents. This is especially true when it comes to their financial independence, quality of life, social and inter-personal connections, and employment and housing opportunities — and with good reason.

Autism is a growing public health crisis, with millions of families desperate for solutions and resources. Easter Seals and others in the autism community are doing their best, but current systems, structures and resources to help people with autism and their families do not adequately meet the growing need, especially for adults with autism.

“The study quantifies what we’ve heard anecdotally over the years,” says Patricia Wright, Ph.D., MPH, Easter Seals national director, autism services. “The one consistent message Easter Seals hears from the families we serve — after the initial apprehension and anxiety of learning their child has autism — is an overwhelming concern about the life-long supports their child with autism may need to be independent.”

Study Shows Parents’ Hope for Independence . . . Financial and Otherwise
The nationwide study provides new insight into the ongoing challenges facing individuals and families living with autism, particularly their concerns about the future. It’s unique in that it closely considers and quantifies the very real concerns of parents of children with autism in relation to parents of typically developing children.

A sampling of the findings:

• Parents of children living with autism are very concerned about their children fitting into society, with very few feeling their children will be able to:
  • Make his or her own life decisions (14% compared to 65% of parents with typically developing children)
  • Have friends in the community (17% compared to 57% of typical parents)
  • Have a spouse or life partner (9% compared to 51% of typical parents)
  • Be valued by their community (18% compared to 50% of typical parents)
  • Participate in recreational activities (20% compared to 50% of typical parents)
• Children with autism also are less likely than their typically developing peers to have bank accounts (37% vs. 55%) and use electronic products like cell phones (9% vs. 41%) or MP3 players (23% vs. 49%) — all tools of mainstream society.
• Many parents of children with autism report they’re “financially drowning,” with concerns for their children’s financial independence seeming to far surpass the worries of typical parents. Seventy-four percent of parents of children with autism fear their children will not have enough financial support after they die, while only 18% of typical parents share this fear.

  They also express extreme financial strains and costs associated with caring for a child with autism, with more than half stating that the cost of caring for my child:

  • Drains my family’s current financial resources (52% compared to 13% of typical parents)
  • Will drain my family’s future finances (50% compared to 10% of typical parents)
  • Will cause me to fall short of cash during retirement (54% compared to 13% of typical parents)
• Key to adult independence is employment, yet only 24% of teenagers with autism have looked for a job, compared to 77% of their typically developing peers. And 76% of parents of children with autism are concerned about their child’s future employment, when only 35% of typical parents share this fear.

“Families living with autism face so many challenges on a daily basis,” says John Chandler, senior vice president and chief marketing officer of MassMutual’s U.S. Insurance Group. “But this study has really brought home for us how much stress they face when it comes to their current financial situation, the future of their child with autism, their other children and their own retirement. Our hundreds of Special Care Planners across the country are in a great position to help make at least this part of their struggle easier.”

As an Easter Seals corporate partner and the study sponsor, MassMutual is committed to serving people living with autism and other disabilities through its exclusive SpecialCareSM program, an innovative solution that gives families with individuals with special needs access to information, specialists, and financial strategies that can help improve their quality of life.

Easter Seals worked with Harris Interactive, and in cooperation with the Autism Society of America, to conduct the Living with Autism Study and survey 1,652 parents of children who have autism and 917 parents of typically developing children about daily life, relationships, independence, education, housing, employment, finances and healthcare.*

Study Findings to Drive Solutions
“Easter Seals strives to make data-based-decisions,” Wright says. “With this study, the disparities that parents of typically developing children and parents of children with autism experience can now be shared via solid numbers.”

Easter Seals will use the study results to raise awareness of and advocate for the life-long services millions of families living with autism desperately need — including school to work transitions, employment support, residential and community support, and financial planning.

“For parents of kids with autism, there are no simple answers,” adds Wright. “There is an urgent need for increased funding and services — especially for adults with autism. Easter Seals wants to help change all of this and make a difference for families living with autism today.”

*Methodology
This Easter Seals’ Living with Autism Study was conducted online within the United States by Harris Interactive on behalf of Easter Seals between June 16 and July 17, 2008 among 1,652 parents of children age 30 and under who have autism and 917 parents of typically developing children age 30 and under. No estimates of theoretical sampling error can be calculated; a full methodology is available.

About Easter Seals
Autism is a lifelong disability that affects the way a person’s brain functions, involving challenges in communication, social skills, and behaviors. While there is no known cause or cure, autism is treatable and people with autism can — and do — lead meaningful lives. Easter Seals is the leading non-profit provider of services for individuals with autism, developmental disabilities, physical disabilities and other special needs. For nearly 90 years, we have been offering help and hope to children and adults living with disabilities, and to the families who love them. Through therapy, training, education and support services, Easter Seals creates life-changing solutions so that people with disabilities can live, learn, work and play. Visit www.easterseals.com or http://www.actforautism.org/ to learn more about autism, find services at an Easter Seals near you, or help change the lives of people living with autism by becoming a donor or volunteer.

About Harris Interactive®
Harris Interactive is a global leader in custom market research. With a long and rich history in multimodal research that is powered by our science and technology, we assist clients in achieving business results. Harris Interactive serves clients globally through our North American, European and Asian offices and a network of independent market research firms. For more information, please visit http://www.harrisinteractive.com/.

About MassMutual Financial Group
MassMutual is a leader in helping people with disabilities and other special needs and their families through its exclusive SpecialCareSM Program, an innovative outreach initiative that provides access to information, specialists, and financial solutions that can help improve the quality of life for people with disabilities and other special needs and their families and caregivers. For more information and resources on autism, go to www.massmutual.com/autism.

MassMutual Financial Group is a marketing name for Massachusetts Mutual Life Insurance Company (MassMutual) and its affiliated companies and sales representatives. MassMutual and its subsidiaries had more than $500 billion in assets under management at year-end 2007. Assets under management include assets and certain external investment funds managed by MassMutual’s subsidiaries. Founded in 1851, MassMutual is a mutually owned financial protection, accumulation and income management company headquartered in Springfield, Mass. MassMutual’s major affiliates include: OppenheimerFunds, Inc.; Babson Capital Management LLC; Baring Asset Management Limited; Cornerstone Real Estate Advisers LLC; The First Mercantile Trust Company; MML Investors Services, Inc., member FINRA and SIPC (http://www.finra.org/ and http://www.sipc.org/); MassMutual International LLC and The MassMutual Trust Company, FSB. MassMutual is on the Internet at http://www.massmutual.com/.

About the Autism Society of America (ASA)
ASA, the nation’s leading grassroots autism organization, exists to improve the lives of all affected by autism. We do this by increasing public awareness about the day-to-day issues faced by people on the spectrum, advocating for appropriate services for individuals across the lifespan, and providing the latest information regarding treatment, education, research and advocacy. For more information, visit http://www.autism-society.org/.

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I found this on the Easter Seals site and suggest  visiting their site for more in depth information on Autism and Services needed for children on the spectrum.

Easter Seals — helping people with disabilities gain greater independence

Easter Seals provides exceptional services, education, outreach, and advocacy so that people living with autism and other disabilities can live, learn, work and play in our communities.
Understanding Speech and Hearing Therapy

Speech and hearing therapy (also known as speech-language pathology and audiology) are important health-related specialties concerned with normal development of human communication and treatment of its disorders. Speech therapy focuses on voice and speech-language skills, while hearing therapy deals with hearing and hearing impairment.

Speech or language disorders may be present at birth or acquired later in life by disease, illness, head injury, substance abuse or allergy.

Hearing loss may be acquired before or during birth if a pregnant woman takes certain drugs or contracts a viral disease such as rubella (German Measles). Children sometimes acquire hearing loss from infection and inflammation of the middle ear or from communicable diseases. Adult hearing may be affected by prolonged exposure to loud noise and the process of aging.

Who Needs Speech-Language Pathology and Audiological Services?

Speech-Language Pathology is used to help:

* Individuals with voice disorders to develop proper control of their vocal and respiratory systems
* Individuals who stutter to learn to cope with the disorder and increase fluency
* Individuals with aphasia (a condition in which an individual has difficulty expressing thoughts and understanding others) as a result    of a stroke or head injury. Speech-language pathology helps individuals relearn language and speech skills.
* Children and young adults with language disorders

Audiological services are used to:

* Determine existence and type of hearing impairments
* Provide rehabilitative services
* Assess amplification devices, such as hearing aids
* Teach individuals ways in which they can make the best use of their remaining hearing

Speech and hearing therapists, recognized as speech-language pathologists and audiologists, who provide treatment are professionally trained specialists holding master’s degrees or the equivalent from programs accredited by an Educational Standards Board of the American Speech-Language-Hearing Association (ASHA).

Some speech-language pathologists and audiologists hold doctoral degrees and work as teachers, advisors, researchers and consultants. Some specialize in certain areas, such as aphasia or hearing disorders in children, or participate in prevention and early identification programs.

Speech-language pathologists who use the initials “CCC-SLP” after their name have passed a national examination administered by the Clinical Certification Board of ASHA. Audiologists who pass a different national test, administered by the board, receive a Certificate of Clinical Competence in Audiology and qualify to use the initials “CCC-A” after their name. A person who meets requirements in both professional areas may be awarded both certificates.

Individualized Treatment Plans

A speech-language pathologist evaluates a person’s speech-language skills, determines the probable cause and extent of any existing disorder and develops appropriate treatment to correct or lessen the communication problem. Clinical methods used depend on the nature and severity of the problem, the age of the client and the client’s awareness of the problem.

An audiologist, after evaluating a person’s hearing and determining the type of hearing loss, establishes a treatment plan. This may involve therapy, prescription of special equipment such as hearing aids and electronic communication devices and referral for possible surgery or medication.

Visit the Easter Seals site for more information

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Psychologist Simon Baron-Cohen and his colleagues at Cambridge’s Autism Research Centre have created the Autism-Spectrum Quotient, or AQ, as a measure of the extent of autistic traits in adults. In the first major trial using the test, the average score in the control group was 16.4. Eighty percent of those diagnosed with autism or a related disorder scored 32 or higher. The test is not a means for making a diagnosis, however, and many who score above 32 and even meet the diagnostic criteria for mild autism or Asperger’s report no difficulty functioning in their everyday lives. You can take the test here.

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Autism Speaks, the nation’s largest autism science and advocacy organization, and Unlock Autism today applauded Representatives Mike Doyle (D-PA), Chris Smith (R-NJ), Eliot Engel (D-NY), and Hank Johnson (D-GA) for their introduction of a House companion bill to the Senate’s Autism Treatment Acceleration Act (ATAA), which was introduced last month by Senators Richard Durbin (D-IL), Robert Casey (D-PA), and Robert Menendez (D-NJ). Like the Senate version, the House version of the ATAA (H.R. 2413) is comprehensive federal legislation that addresses several critical challenges facing the autism community, including increased funding for scientific research, treatment and services. The ATAA incorporates provisions from the Expanding the Promise of Individuals with Autism Act (EPIAA), originally proposed by Representatives Doyle, Smith, Engel, and former-Representative Chip Pickering.

A welcome sign of relief  to many who routinely spend $30-$50k on therapy’s – not even considered for reimbursement by insurance companies.

As in the Senate’s ATAA bill, a key section of the House bill requires all insurance companies to provide coverage for the diagnosis and treatment of autism spectrum disorder (ASDs), including coverage of Applied Behavior Analysis (ABA) therapy – a medically-necessary, evidence-based autism treatment. While the number of states that have enacted comprehensive autism insurance reform legislation has grown to ten, most state insurers are still allowed to specifically exclude coverage for these critical services, which can cost upward of $50,000 a year – well beyond the means of most families.

The House version of the bill also addresses the unique needs of adults with ASDs, creating a demonstration project with one-year planning grants and multi-year implementation grants for the provision of service for adults with autism. In addition, it creates the Network for Autism Spectrum Disorders Research and Services aimed at accelerating the dissemination and utilization of critical, new information, moving it from “bench to bedside” as quickly as possible.

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Although in it’s too early, this Autism Fever and the Brain research is very promising and holds a lot of hope for Autism sufferers.

ScienceDaily (Apr. 2, 2009) – Scientists at Albert Einstein College of Medicine of Yeshiva University have proposed a sweeping new theory of autism that suggests that the brains of people with autism are structurally normal but dysregulated, meaning symptoms of the disorder might be reversible.

The central tenet of the theory, published in the March issue of Brain Research Reviews, is that autism is a developmental disorder caused by impaired regulation of the locus coeruleus, a bundle of neurons in the brain stem that processes sensory signals from all areas of the body.

The new theory stems from decades of anecdotal observations that some autistic children seem to improve when they have a fever, only to regress when the fever ebbs. A 2007 study in the journal Pediatrics took a more rigorous look at fever and autism, observing autistic children during and after fever episodes and comparing their behavior with autistic children who didn’t have fevers. This study documented that autistic children experience behavior changes during fever.

“On a positive note, we are talking about a brain region that is not irrevocably altered. It gives us hope that, with novel therapies, we will eventually be able to help people with autism,” says theory co-author Mark F. Mehler, M.D., chairman of neurology and director of the Institute for Brain Disorders and Neural Regeneration at Einstein.

Autism is a complex developmental disability that affects a person’s ability to communicate and interact with others. It usually appears during the first three years of life. Autism is called a “spectrum disorder” since it affects individuals differently and to varying degrees. It is estimated that one in every 150 American children has some degree of autism.

Einstein researchers contend that scientific evidence directly points to the locus coeruleus-noradrenergic (LC-NA) system as being involved in autism. “The LC-NA system is the only brain system involved both in producing fever and controlling behavior,” says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.

The locus coeruleus has widespread connections to brain regions that process sensory information. It secretes most of the brain’s noradrenaline, a neurotransmitter that plays a key role in arousal mechanisms, such as the “fight or flight” response. It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another). Poor attentional focusing is a defining characteristic of autism.

“What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks,” says Dr. Mehler.

Drs. Purpura and Mehler hypothesize that in autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors (chemical substances both within as well as outside the genome that regulate the expression of genes). They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.

As evidence, the researchers point to a 2008 study, published in the Journal of Autism and Developmental Disorders, that found a higher incidence of autism among children whose mothers had been exposed to hurricanes and tropical storms during pregnancy. Maternal exposure to severe storms at mid-gestation resulted in the highest prevalence of autism.

Drs. Purpura and Mehler believe that, in autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function. “This could not happen if autism was caused by a lesion or some structural abnormality of the brain,” says Dr. Purpura.

“This gives us hope that we will eventually be able to do something for people with autism,” he adds.

The researchers do not advocate fever therapy (fever induced by artificial means), which would be an overly broad, and perhaps even dangerous, remedy. Instead, they say, the future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

“If the locus coeruleus is impaired in autism, it is probably because tens or hundreds, maybe even thousands, of genes are dysregulated in subtle and complex ways,” says Dr. Mehler. “The only way you can reverse this process is with epigenetic therapies, which, we are beginning to learn, have the ability to coordinate very large integrated gene networks.”

“The message here is one of hope but also one of caution,” Dr. Mehler adds. “You can’t take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it – that’s folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way.”

Science Daily is an excellent site for Autism related research, support them so they can support us..

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The development, maintenance, and repair of myelin is the single most important factor affecting cognition and behavior, according to a UCLA neurology professor who has collected extensive data on the nerve insulator. In an article to be published in an upcoming issue of Biological Psychiatry, George Bartzokis, MD, asserts that myelin may be the universal cause or contributor to a wide range of neuropsychological brain disorders, from autism to Alzheimer’s disease. Dr. Bartzokis, who directs the UCLA Memory Disorders and Alzheimer’s Disease Clinic in Los Angeles, suggests that using noninvasive imaging technology to view the miles of myelin in the brain as it grows and breaks down throughout a human life cycle may offer insights leading to the development of new treatments for brain disorders. Nicotine, which studies have suggested enhances the growth and maintenance of myelin, could be one such novel treatment.

In some of the first research to approach brain disorders from a myelin-centered point of view, Dr. Bartzokis studied the effects of cholinergic treatments, including acetylcholinesterase inhibitors (AChEIs) that are used to improve a neuron’s synaptic signaling in people with diseases such as Alzheimer’s. Some data suggest that such treatments may even modify or slow the progression of Alzheimer’s as well as other diseases.

Nicotine, Age, and Disease

Dr. Bartzokis hypothesizes that cholinergic stimulation at neuronal synapses affects the myelination process throughout brain development in the course of a human’s lifetime.He found in clinical trials that cholinergic treatment protects brain cells, while postmortem and imaging data have shown cholinergic receptor changes during brain development and degeneration. Trials have also revealed epidemiologic evidence that nicotine from tobacco may have a protective effect on degenerative diseases of old age and younger psychiatric populations. Cholinergic treatments have also shown efficacy in the aging process and age-related neurodegenerative diseases such as Alzheimer’s disease, as well as some neurodegenerative diseases like autism and ADHD.

According to Dr. Bartzokis, myelination development resembles an inverted “U” over the course of a lifetime, with increasing myelin development peaking in middle age and breaking down and declining in later years. Following the analogy of the Internet, Dr. Bartzokis says the “connectivity” provided by myelination increases speed by 10-fold and decreases refractory time by 34-fold. Thus, myelination increases the “bandwidth,” or processing capacity, of our brain’s Internet by 340-fold and is “indispensable for developing our uniquely elaborate higher cognitive functions.”

Different cortical regions myelinate at different ages, with later-myelinating oligodendrocytes growing increasingly more complex as we age. Irregular development during the most complex stages of the myelination process contributes to several of the neuropsychiatric disorders that tend to manifest in the early years. These disorders—eg, autism, ADHD, schizophrenia, mood disorders, addictions—are defined by overlapping cognitive and behavioral symptom clusters.

According to Dr. Bartzokis, healthy individuals with normal myelin development typically lose 45% of their myelinated fiber length when they reach the degeneration phase in adulthood. This change in the brain may cause progressive losses of memory and cognitive functions, as well as mild to severe behavioral changes.

The loss of myelin and its components such as sulfatide, myelin basic protein, and cholesterol begins early in the development of Alzheimer’s disease, well before diagnosis of dementia or mild cognitive impairment. The myelin breakdown process is further modified by risk factors such as the presence of APOE ε4 or environmental factors such as a head trauma.

Nicotine’s Effect on Myelination and Repair

Recent research has unveiled some surprising findings on the influence of nicotine on myelination and the aging process. Direct nicotinic stimulation associated with smoking has been shown to increase nicotinic receptors in the late myelinating frontal and temporal intracortical regions. Unlike most agonists, nicotine causes an up-regulation of its receptors and has been shown to accelerate brain function recovery when white matter is damaged.

Nicotine dependence is common among people with psychiatric disorders. Some researchers have suggested the high prevalence of nicotine use among the psychiatric population represents an unconscious effort to “self-medicate.” Research on proteins has suggested that nicotine may marginally increase the expression of myelin proteins; other addictive drugs (eg, cocaine, alcohol) along with developmental diseases (eg, schizophrenia, bipolar disorder, depression) show a decrease of these proteins.

Other research has found an association between nicotinic stimulation and protective effects in schizophrenia and autism, where cortical myelination deficits have been documented. While nicotine has well-known negative effects on overall health, smoking during later years is also associated with a reduced likelihood of the development of degenerative conditions like Alzheimer’s and Parkinson’s diseases. Using the myelin-centered model, the apparent beneficial aspects of smoking on brain disorders can be attributed to nicotine’s stimulation of oligodendrocyte precursors. Dr. Bartzokis believes that nicotine, delivered through a patch, not through smoking cigarettes, should be studied for its efficacy in promoting the growth and maintenance of myelin, and that AChEIs “deserve much closer scrutiny” as a therapy for the prevention of both developmental and degenerative brain disorders.

—Kathlyn Stone http://www.neuropsychiatryreviews.com/07jan/myelin.html

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Looks like we are making progress..

President-Elect Obama has drafted comprehensive autism legislation, including a section addressing a broad based federal autism insurance mandate.

In his Presidential campaign statement on Autism Spectrum Disorders, President-Elect Obama committed to bringing autism insurance reform to the entire nation. The statement stated that Obama and Biden “will mandate insurance coverage of autism treatment and will also continue to work with parents, physicians, providers, researchers, and schools to create opportunities and effective solutions for people with ASD.” For the complete campaign statement, and to read the draft legislation, go to http://www.autismvotes.org.

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Please be true to your word and fund more in depth research regarding the causes and prevention of Autism

and other PDD’s   1 in 150 is an epidemic of the worst proportions as it affects defenseless children and can destroy families, wreak hvvac on local school board budgets and community taxes. We need solutions now.

Here are some suggestions, Investigate and report back within 12 months time any connection regarding

- Plastic PBA’s, Cell Phone Signals and Mercury laced shots

- Providing economic support for families who actively seek and complete therapy’s currently not covered under health insurance

- Providing economic support on a per child basis still in the school system for providing a more precise and personalized education platform and goals to work towards. I do well for my family but paying $10-$25,000 for treatments, or more per year is just a bit too much to afford.

- Increasing regulation and oversight over Autism related treatments, too much hope being sold with snake oil out there

- Creating a national database of what works for which conditions best, right now its trial and error over and over again

- Provide $10 billion in funding Autism research asap, at both the commercial and holistic levels.

12 months is aggressive, but we need to fast track this as it continues to grow in numbers both in terms of those afflicted, and those it affects.

Do it Barrack, help our children and make this your legacy while still in office, not in the last few weeks of office.  Do it now..

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You know, I had heard it was a disgruntled ex employee of a Pharmaceutical company that started this whole MMR connection, if that is true this person should be tarred an feathered and tied to a whipping post in the village square for wasting so many valuable years of research down a wrong street, years that could have been used to find a cause and cure. Instead, we have wasted big time dollars and time accusing and defending.. What a shame, Now this article appeared int he NY Times claiming that the researchers had a conflict of interest who published the findings.. all this for what, a Gov’t grant or a mention in some Journal?

“Meanwhile, the original paper’s publisher — The Lancet — complained in 2004 that the lead author had concealed a conflict of interest. Ten of his co-authors retracted the paper’s implication that the vaccine might be linked to autism. Three of the authors are now defending themselves before a fitness-to-practice panel in London on charges related to their autism research.

Sadly, even after all of this, many parents of autistic children still blame the vaccine. The big losers in this debate are the children who are not being vaccinated because of parental fears and are at risk of contracting serious — sometimes fatal — diseases.”

How about we shift towards researching things introduced into the environment that mirror the rise of Autism, Such as; Cell Phones, PC’s, Plastic Everything, Teflon, Hormone use in the food supply, even down to Hydro-Ponic Marijuana. Doesnt anyone else wonder about these things and their possible place in the cause of the Autism Epidemic? Anyone there?

Ten years ago, a clinical research paper triggered widespread and persistent fears that a combined vaccine that prevents measles, mumps and rubella — the so-called MMR vaccine — causes autism in young children. That theory has been soundly refuted by a variety of other research over the years, and now a new study that tried to replicate the original study has provided further evidence that it was a false alarm. Read More from this New York Times article

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Came across this video series, http://www.modelmekids.com/autism-videos.html

Anyone ever use it? What were your results? Seems like a great idea and one I have often thought about given my sons love of the video tape, or dvd.

Thanks for sharing… is there anybody out there??

The Time for School video presents social skills in the context of school. It features elementary school-aged children demonstrating appropriate social skills in the classroom, library, on the playground, and in the hallway. Each scene lasts between 30 seconds and 3 minutes, depending on the chapter. At the end of each chapter is a storyboard summarizing the rules taught.

The video is hosted by a young boy, who narrates each scene.

With narration: In the first half of the video, the visual is combined with narration and graphics that help explain the particular rule.

Without narration: In the second half of the video, the same video is repeated without narration and graphics. This allows a parent, Autism teacher, or therapist to customize the lesson the individual child and/or to test what was learned in the first viewing of the video.

Each social skill is demonstrated in more than one situation and across environments. This is useful to children with Autism and Asperger’s Syndrome because it helps with generalization of the skill taught.

Graphics and music are used to make the video appealing to children with Autism, Asperger’s Syndrome, and Nonverbal Learning Disorders. A high production value helps keep the child’s interest so that he or she will want to watch many times.

Check it out here

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Research: “The Myelin Project”:

The exciting work of researchers funded by The Myelin Project, whose goal is to remyelinate the human central nervous system, may someday have benefits for autistic children. Only time will tell if a specific area of damaged neurons can be found and potentially repaired with stem cells.

The first human trial, conducted by Dr. Timothy Vollmer at Yale University School of Medicine, will attempt to transplant myelin-forming Schwann cells into the brains of five patients with multiple sclerosis. The cells will be obtained from the sural nerves of the patients themselves. Although Schwann cells normally produce myelin in the peripheral nervous system, several recent experiments conducted on rodents and cats have shown these cells have the ability to remyelinate in the CNS as well.

While multiple sclerosis is a long way from autism, there is discussion of anti-myelin antibodies in autism, and there is talk of inflammatory processes involving myelin. Whether this technology can help autism if it works for multiple sclerosis is anybody’s guess, but it’s exciting to wonder about.

The Myelin Project funds a Cell Culture Unit at the University of Wisconsin-Madison, where Dr. Su-chun Zhang continues to generate cultures with ever-higher percentages of human oligodendrocyte precursors (OPs). Oligodendrocytes are the cells that normally myelinate the CNS. If obtainable in sufficient quantity, they would provide an alternative to Schwann cells for transplantation. The Unit has developed a method to track transplanted OPs by MRI, labeling the cells with iron particles. In another recent experiment, Dr. Baron-Van Evercooren and colleagues were able to remyelinate as many as 55% of the nerves in monkey spinal cord lesions by transplanting the monkeys’ own Schwann cells. These initial positive results, however, have not been confirmed in subsequent attempts. She suspects that the viral labels she used to distinguish the transplanted cells caused them to die. She is trying again without viral labeling. If successful, this experiment would prove that CNS remyelination is feasible in higher animals.

Several researchers funded by The Myelin Project have injected myelin-forming cells into the ventricles of the brain of experimental animals and have shown that these cells were transported by the cerebrospinal fluid to all regions of the brain. This makes it more likely that injected cells will travel to where the myelin needs to be repopulated.

The Myelin Project has funded Dr. Oliver Br�stle of the University of Bonn, Germany, and Dr. Evan Snyder of Harvard University to work with neural stem cells (NSC). These are self-renewing, multipotent cells, capable of differentiating into the major types of neural cells, including oligodendrocytes. One of their most potentially beneficial properties is their tendency to respond to signals in the CNS environment. In CNS diseases, these signals guide the cells to damaged areas. Second, they prompt them to differentiate into the specific cell type needed for the repair — neurons in nerve diseases like Parkinson’s and oligodendrocytes in myelin disorders like the leukodystrophies and multiple sclerosis.

NSCs are typically of fetal origin, but have also been found in the adult brain. NSCs can be multiplied in culture indefinitely as an “immortal” cell line. They could eventually provide an inexhaustible source of myelin-forming cells, eliminating the need for obtaining them from fresh tissue. Several research centers are now testing human NSCs to verify their safety and in particular to rule out any risk of their becoming cancerous. If this testing concludes favorably, then prospective myelin repair strategies could take a two-fold approach. NSCs would be injected into the ventricular system where the cerebrospinal fluid would circulate them to all parts of the CNS. Local signals would then come into play, guiding the cells to the specific demyelinated areas.

The Myelin Project has also funded Dr. Robin Franklin of the University of Cambridge to study olfactory ensheathing cells, a third type of myelin-producing cell. He has perfected a technique for demyelinating the area of rat brain connecting the cerebellum with the brain stem. He subsequently remyelinated the area by transplanting rat Schwann cells, which adds to the body of evidence in favor of Schwann cell transplantation as a way of repairing CNS myelin lesions.

The Myelin Project has also funded Dr. Inderjit Singh of the Medical University of South Carolina to study the use of Lovastatin in the treatment of myelin disorders. The drug corrects the biochemical defect of adrenoleukodystrophy, lowering the levels of very long chain fatty acids in plasma. Preliminary studies with an animal model of MS have confirmed Lovastatin’s ability to block the induction of cytokines, substances responsible for the inflammation of the CNS. We know that the levels of very long chain fatty acids and of some cytokines are elevated in autism. I am wonderijng already if Lovastatin might be worth trying for children with documented elevated very long chain fatty acids and elevated cytokines.

These studies present exciting possibilities for the future for treating neurodegenerative diseases. They may eventually have relevence for such diverse conditions as autism, cerebral palsy, and CNS vaccine damage syndromes. Time will tell.

find more at http://www.healing-arts.org/children/cell.htm

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Where as I appreciate any and most attention Autism receives, I feel a bit sickened by the fact that celebrity’;s seem to be leanding their names solely for the purpose of publicity.

Jenny is cool, but her book talks about she is able to afford the therapy’s that most of us only dream of or mortgage our homes for.  the therapy’s she mentions in the book are not hers, they are those of Berdard and Tomatis. Deidre Imus was a big factor in passing the Combating Autism Act, which is a lame act of empty promises. Where is she now? Robert Kennedy, now I was shocked to see how much attention he gets for helping Autism get reserach dollars, I thought he was an enviormentalist? And what is President Bill; Clintoln doing rasing money for children in far off lands, most of which wil never even see the dollasr raised when 1 in 150 children in the US are diagnosed with Autism, shame on you Bill! I don’t know, maybe I am wrong here and maybe, just maybe getting celebrity endorsement is better than none, but what have we gained since Autism is such a celebrity cause? A few best sellers or rehashed gobblee goop?

This is not a part time thing here, this is a life long condition and for most finanacial burden. What do we have to do, go on TV and get sponsors for individual families here in the states? We need insurance reforms like we see taking place in a few states like New Jersey, we need the medical community to rally here. Autism is horrible and the numbers climb ever day, why is it not being treated as an epidemic, but rather as a celebrity attention grabber!!?? What are your thoughts. Please share them and lets take the bull by the horns ourselves and Unlock Autism.

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We could use a hand in finding material to share with others like you. If you have an experiences or know of other great resources for information, Please leave some comments or write to us at info@unlockautism.com This site is for us all. We are trying to direct you to pertinent information about Autism. Success stories and information about therapy’s and diets which helped or those which didn’t. Keep in mind, not all therapy’s will work for all. Autistic people are individuals in the truest sense of the word, with loving and caring families trying to unlock autism and let that person out.

If we can gather enough stats and information, perhaps we can help others. For us personally, Its been a whole lot of Love, Therapy’s and at times Snake Oil. Whats worked for us has been, ABA, Signing Time, Auditory Integration and Omega’s plus the usual OT, PT and Speech. But also encouraging more social engagement.

All I know is that we as parents know what works and what doesn’t, lets help those who are just discovering Autism. Let us help each other from being fooled by the latest and greatest therapy’s promising miracle and instant cures.
If you are interested in getting involved with UnlockAutism.com, let us know and share your wisdom.

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Original Article Found on TranslatingAutism.com You can find a more complete description and review of this paper based on the press coverage here. Thus, I’ll limit this to a micro summary and a few related thoughts. The researchers wanted to experimentally test the hypothesis that exposure to maternal neuronal antibodies (IgG) during the PREnatal period could be one of the causes of at least some variants of Autism. To test this hypothesis the researchers exposed 4 prenatal rhesus monkeys with IgG taken from human mothers who had multiple children with ASD. They also exposed 5 prenatal monkeys with IgG taken from human mothers who did not have any children with Autism. Once the monkeys were born, these two groups were also compared to monkeys that had not been exposed to any antibodies. The researchers found that the monkeys that had been exposed to the antibodies of human mothers of children with autism engaged in much higher levels of unique whole-body stereotypic behaviors and less social contact with familiar peers, than did the monkeys exposed to IgG of mothers of typically developing kids or monkeys not exposed to any antibodies. Furthermore, these stereotypic behaviors increased when the monkeys were exposed to novel environments or peers. As I understand how controversial this paper will be for some people, I want to say that the authors are very clear and explicit in stating that this is NOT an animal model of autism. That is, they did not intent to say that they were able to “cause” autism in these monkeys via exposure to IgG. Instead, their data presents some evidence that exposure to IgG before birth leads to unique patterns of stereotypic behaviors, similar to those observed in some children with ASD. This is a very small preliminary study, but the results are fascinating in that it will guide future research to explore exposure to IgG as a potential cause (one of many) of ASD.

Seems plausible since the IgG antibodiy can get through the placenta to protect the baby..but much more work needs to be done first. For more on IgG http://en.wikipedia.org/wiki/IgG

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From Age of Autism – What will happen to the Monkees ?

The first research project to examine effects of the total vaccine load received by children in the 1990s has found autism-like signs and symptoms in infant monkeys vaccinated the same way. The study’s principal investigator, Laura Hewitson from the University of Pittsburgh, reports developmental delays, behavior problems and brain changes in macaque monkeys that mimic “certain neurological abnormalities of autism.”

The findings are being reported Friday and Saturday at a major international autism conference in London.

Although couched in scientific language, Hewitson’s findings are explosive. They suggest, for the first time, that our closest animal cousins develop characteristics of autism when subjected to the same immunizations – such as the MMR shot — and vaccine formulations – such as the mercury preservative thimerosal — that American children received when autism diagnoses exploded in the 1990s.

The first publicly reported results of this research project come in both oral and poster presentations on Friday and Saturday at the International Meeting For Autism Research in London. Poster presentations must go through a form of peer review before they are presented at the conference; the papers have not yet appeared in a scientific journal.

In addition to Hewitson’s oral presentation today, on Saturday in one of two related poster presentations, the researchers also are reporting in their abstract that “vaccinated animals exhibited progressively severe chronic active inflammation [in gastrointestinal tissue] whereas unexposed animals did not. We have found many significant differences in the GI tissue gene expression profiles between vaccinated and unvaccinated animals.” Numerous scientific studies, as well as many parents, report severe GI ailments in children with regressive autism.

The results are sure to be controversial, in part because they lend credence to studies first published in 1998 by British pediatric gastroenterologist Andrew Wakefield, one of Hewitson’s co-authors on these findings. He described an unusual inflammatory bowel condition in children who had regressed into autism after they received the measles-mumps-rubella (MMR) vaccination. Wakefield is currently fighting charges of medical misconduct in Britain over allegations of conflict-of-interest and improper procedures related to that paper. He denies the charges.

In the program for the conference, the 7th Annual International Meeting for Autism Research (IMFAR), there are three separate presentations listed that report results from the overall research program. The first, an oral presentation entitled “Pediatric Vaccines Influence Primate Behavior, and Amygdala Growth and Opioid Ligand Binding” (the “amygdala abstract”) was led by Dr. Hewitson and lists 12 co-authors, including five of her colleagues from the University of Pittsburgh and Dr. Wakefield. Other authors are chemists, pathologists and psychologists from the universities of Kentucky, California-Irvine, and Washington.

Hewitson’s introductory presentation will be followed by two poster presentations on Saturday; one of the two, “Pediatric Vaccines Influence Primate Behavior, and Brain Stem Volume and Opioid Ligand Binding”, was led by Wakefield and includes six additional co-authors.

It focuses on the developmental effect of vaccine exposures on brain growth during infancy. The second, “Microarray Analysis of GI Tissue in a Macaque Model of the Effects of Infant Vaccination,” was led by Steven Walker of Wake Forest University and performed gene array analysis on the intestinal tissues of the vaccinated and unvaccinated monkeys.

The studies address – albeit in animals, not children — one of the major criticisms by parents and scientists concerned about a possible link between the greatly stepped-up immunization schedule in the 1990s, including higher exposure to the mercury preservative, and autism. While the Food and Drug Administration approves individual vaccines as safe and effective, and an advisory committee to the Centers for Disease Control and Prevention recommends the childhood immunization schedule adopted by the states, the overall health outcomes from the total vaccine load, versus no vaccinations at all, have never been compared, the authors said.

A bill requiring the government to conduct a study of autism rates in unvaccinated American children is pending in the U.S. House of Representatives, co-sponsored by Reps. Carolyn Maloney (D-N.Y.) and Tom Osborne (R.-Neb.). Just this week, former National Institutes of Health Director Bernadine Healy called for more research into a possible vaccine link to autism and said the question had not been settled, despite repeated assertions to that effect by the CDC, the Institute of Medicine and the American Academy of Pediatrics.

In the abstract for today’s oral presentation, the authors noted that macaques, the type of monkey used in the study, “are commonly used in pre-clinical vaccine safety testing, but the combined childhood vaccine regimen, rather than individual vaccines, has not been studied. Childhood vaccines are a possible causal factor in autism, and abnormal behaviors and anomalous amygdala growth are potentially inter-related features of this condition.”

The study found evidence of both behavioral and biological changes after the 13 macaque monkey infants were administered proportional doses, adjusted for age, of the vaccines recommended between 1994 and 1999. Three monkeys were not given any vaccines.

“Primate development, cognition and social behavior were assessed for both vaccinated and unvaccinated infants using standardized tests developed at the Washington National Primate Research Center.” MRI and PET scans looked for brain changes after administration of the MMR.

“Compared with unexposed animals, significant neurodevelopmental deficits were evident for exposed animals in survival reflexes, tests of color discrimination and reversal, and learning sets,” the authors reported. “Differences in behaviors were observed between exposed and unexposed animals and within the exposed group before and after MMR vaccination. Compared with unexposed animals, exposed animals showed attenuation of amygdala growth and differences in the amygdala binding of [11C]diprenorphine. Interaction models identified significant associations between specific aberrant social and non-social behaviors, isotope binding, and vaccine exposure.”

One of the Saturday abstracts makes the further point that the research “revealed significant differences between exposed and unexposed animals” in the kinds of developmental behaviors a mother might be able to observe, “with delayed acquisition of root, suck, clasp hand, and clasp foot reflexes.” They conclude by noting that “This animal model examines the neurological consequences of the childhood vaccine regimen, Functional and … brainstem anomalies were evident in vaccinated animals that may be relevant to some aspects of autism. The findings raise important safety issues while providing a potential animal model for examining aspects of causation and disease pathogenesis in acquired neurodevelopmental disorders.”
–
Dan Olmsted is Editor of Age of Autism.

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Researchers from the Massachusetts Institute of Technology (MIT) have recently generated a mice model for autistic savants – a phenomenon in which an autistic person has an outstanding skill alongside his poor ability in social interactions. By using genetically engineered mice in which a specific protein in the brain was inactive, the researchers discovered an enhanced learning ability of the mice, but also an impaired long term memory, which resembles autism characteristics. The scientists hope that in the future, this work will lead to the development of treatment for autism and for other brain development disorders.
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Seems a bit like covering one’s tracks here. Seizures and Autism commonly go – hand in hand and can trigger serious health issues which lie dormant in the body.

Written and owned By Michael Smith, North American Correspondent, MedPage Today Published: March 14, 2008

Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston.

ATLANTA, March 14 — An apparent increased risk of febrile seizures has led the CDC to soften one of its recommendations on immunizing children against measles, mumps, rubella, and varicella with a combination vaccine.

The agency had said the combination tetravalent vaccine against the four diseases (ProQuad) was to be preferred over vaccination with a trivalent measles, mumps, and rubella vaccine at the same time as a separate varicella shot.

That preferential recommendation has been withdrawn. The agency’s Advisory Committee on Immunization Practices (ACIP) now says there should be no preference, the CDC said in the March 14 issue of Morbidity and Mortality Weekly Report.

The change comes after review of data from the Vaccine Safety Datalink, which monitors vaccine safety, as well as preliminary results from a post-licensing study conducted by Merck, which makes the tetravalent vaccine.

The Vaccine Safety Datalink, the CDC said, showed a signal of increased risk for seizure among children ages 12 to 23 months who were given the tetravalent vaccine, compared with those who got the trivalent vaccine.

The increased rates were seen seven to 12 days after vaccination.

Once the signal was seen, the agency said, analysts used the Vaccine Safety Datalink for a study comparing seizure rates among children who got the tetravalent vaccine and those who got a trivalent vaccine plus a varicella vaccine at the same visit.

The analysis included 43,353 children ages 12 to 23 months who received the tetravalent vaccine and 314,599 who received the trivalent vaccine and varicella vaccine at the same visit.

The researchers reviewed medical records to validate the diagnosis and used a multivariate logistic regression to adjust for age and influenza season, the CDC said.

Results of that analysis showed:

* A rate of nine febrile seizures per 10,000 vaccinations among recipients of the tetravalent vaccine.
* The rate was four per 10,000 vaccinations among those who got the trivalent vaccine along with the varicella vaccine.
* The adjusted odds ratio was 2.3, with a 95% confidence interval from 1.6 to 3.2, which was significant at P<0.0001.
* Of the 166 children who had febrile seizures after vaccination and had hospitalization information available, 26 (or 16%) were admitted to a hospital.
* There were no deaths.

The advisory committee was told that interim data from the Merck post-licensing study showed a similar relative risk for seizure, although the difference did not reach statistical significance. Only about half of the final sample size needed was available for the analysis.

Neither study looked at the risk of a febrile seizure after the second recommended dose of the vaccine, at ages four through six years.

The CDC noted that the tetravalent vaccine is currently in short supply in the U.S., because of manufacturing problems not related to safety, and is not expected to be widely available before 2009.

The agency also said that febrile seizures are not uncommon in children and generally have an excellent prognosis.

Additional source: CDC
Source reference:
CDC “Update: Recommendations from the Advisory Committee on Immunization Practices (ACIP) regarding administration of combination MMRV vaccine” MMWR 2008; 57(10): 258-60.

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By Todd Neale, Staff Writer, MedPage Today
Published: February 07, 2008
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston.

LONDON, Feb. 7 — A community-based case-control study found no relationship between the measles-mumps-rubella (MMR) vaccine and autism spectrum disorders, researchers reported here.

“No difference was detected in the distribution of measles antibody or in measles virus in [autism spectrum disorder] cases and controls whether the children had received the first, second, or both MMR vaccinations,” Gillian Baird, Ph.D., of Guy’s and St Thomas’ NHS Foundation Trust, and colleagues wrote online in the Archives of Disease in Childhood.

This study reinforces the findings of two case-control studies published last year and three epidemiological studies published since 1999 that also failed to make any connection between the vaccine and autism spectrum disorders.

Analyzing a cohort of children born from July 1, 1990 through Dec. 31, 1991 in the South Thames region of England, the researchers tested the hypothesis that the MMR vaccine contributed to the pathogenesis of autism spectrum disorders, “as evidenced by signs of a persistent measles infection or abnormally persistent immune response.”

Using various diagnostic criteria, Dr. Baird’s team recruited 98 children with autism spectrum disorders. They were divided into those with broad disorders (66) and those with narrow autism (32).

The researchers also recruited two control groups. One comprised 52 children with special educational needs but no signs of autism spectrum disorders, and the other, 90 children who were developing normally.

All participants had blood drawn and all had had at least one MMR vaccination.

The researchers tested for a persistent measles infection in peripheral blood mononuclear cells because viral replication occurs here during acute infection and has been reported to contain measles genome in a small number of autistic children. They used three reverse transcriptase PCR assays. Samples were tested to ensure that they were adequate by using a β2 microglobulin housekeeping gene PCR with a sensitivity of 10 genome copies per reaction mixture.

All samples were negative for the first two assays. On one of the assays — the M gene PCR — three samples were reactive for measles virus, with one sample from the narrow autism group containing the C2 strain and two from the normally developing control group containing the D6 strain. All three samples were negative when retested.

The researchers proposed two explanations for the initial positive finding: laboratory cross-contamination or incomplete immunity, which can allow measles virus to be found in asymptomatic people.

Dr. Baird’s team then tested the blood samples for measles IgG antibody with the plaque neutralization test to look for evidence of an abnormal immune response. There was no difference in IgG antibody levels between those with one or two MMR vaccinations (difference=0 log10 (mIU/mL), 95% CI -0.12 to 0.11, P=0.94).

There were no significant differences between the antibody levels in either autism spectrum disorder group or either of the control groups (P=0.13). Differences did not reach statistical significance when those with one or two vaccinations were analyzed separately (P=0.20 and P=0.66, respectively).

The combined control group of special educational needs and normally developing children did not have significantly lower levels of antibodies than those for the narrow autism (P=0.45), broad disorder (P=0.29), or combined autism/broad disorder (P=0.27) groups.

Some level of regression — either the loss of five or more words used communicatively during a three-month period or a regression of words or skills in communication or play behavior — was reported in 23 children in the broad disorders group but antibody levels were not significantly higher than those in the combined control group (P=0.18).

The researchers acknowledged limitations to the study, including the fact that the participants in the normal development control group were not randomly selected.

Also, parents were informed that the study was about MMR vaccination, which may have biased those who signed up to participate.

The researchers noted that only 29% of children with a local diagnosis of autism spectrum disorders received a second MMR vaccination, compared with 50% of those without such a diagnosis, a finding that “is of public health relevance. … This may reflect parental concern about vaccination following a diagnosis of developmental abnormality.”

The study was funded by the Department of Health, the Wellcome Trust, the National Alliance for Autism Research, and Remedi.

Dr. Baird has acted as an expert witness for the diagnosis of autism. Two co-authors have given unpaid advice to lawyers, and another has served as an expert witness, in MMR and MR litigation. Another co-author receives royalties from diagnostic tools used in this study.

Primary source: Archives of Disease in Childhood
Source reference:
Baird G, et al “Measles vaccination and antibody response in autism spectrum disorder” Arch Dis Child 2008; DOI: 10.1136/adc.2007.122937.

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What is SEED?

SEED stands for the Study to Explore Early Development. It is a 5-year, multi-site collaborative study that will help identify what might put children at risk for autism spectrum disorders (ASDs) and other developmental disabilities. It is being conducted by six study sites and a data coordinating center called the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) Network.

What are the six CADDRE centers?

The six CADDRE centers are:

* California CADDRE: Kaiser Permanente Division of Research and the California Department of Health Services
* Colorado CADDRE: Colorado Department of Public Health and Environment and the University of Colorado at Denver and Heath Sciences Center
* Georgia CADDRE: the National Center on Birth Defects and Developmental Disabilities
* Maryland CADDRE: Johns Hopkins University and Kennedy Krieger Institute
* North Carolina CADDRE: University of North Carolina at Chapel Hill
* Pennsylvania CADDRE: University of Pennsylvania School of Nursing and The Children’s Hospital of Pennsylvania

Where exactly is SEED being conducted?

California

a two county area: Alameda and Santa Clara counties

Colorado

the seven-county Denver metropolitan area: (Arapahoe, Adams, Boulder, Broomfield, Denver, Douglas, and Jefferson counties).

Georgia (CDC)

the five-county metropolitan Atlanta area: Clayton, Cobb, DeKalb, Fulton, and Gwinnett counties.

Maryland

seven jurisdictions in northeastern Maryland: Anne Arundel, Baltimore, Carroll, Cecil, Harford and Howard Counties and Baltimore City.

North Carolina

a ten county area: Alamance, Chatham, Davidson, Durham, Forsyth, Guilford, Johnston, Orange, Randolph, and Wake counties.

Pennsylvania

three counties: Chester, Montgomery and Philadelphia counties.

*CDC also funds Michigan State University to run the study’s Data Coordinating Center and Johns Hopkins University to run the study’s central laboratory.

How were the sites selected?

The sites were originally picked through an open competitive review process in 2001 and funded for 5 years. The sites were selected based on the merit of their application. In 2006, CDC had a limited competitive review process and funded the sites for another 5 years.

How can I enroll my child into the study?

The study is a population based study – meaning that the participants will be recruited from all children and families in each study community who meet certain criteria rather then focusing on individuals at a specific clinic or school. Families of children with specific developmental conditions, as well as a random sample of all children born in the community will be invited to participate. If the invited family is interested, then we ask some questions to determine if they are eligible, and if they are eligible then the family is enrolled.

Can I sign my child up for this study?

Although families can self-refer to participate in this study, they have to fulfill certain criteria in order to be eligible. Some families who self refer may not be eligible. Our goal is to send letters of invitation to all families who may fulfill the eligibility criteria. By sending letters of invitation to as many eligible families as possible, we hope to enroll a representative sample of families in each study area.

Examples of the study eligibility criteria include – the child must be born within the study period, the child must be born and still living in the study area, they must have a legal guardian, they must know English or Spanish (although these vary by site), and they must also meet certain diagnostic criteria.

What will each study participant have to do?

Each parent or caregiver will have to answer questions about their child’s development and their family’s medical history. The study clinicians will perform a brief exam and developmental tests on the child. Each parent and child will have to give small samples of blood, cells from inside the mouth, and a sample of the child’s hair. Finally, we would access the mother’s and the child’s medical records.

Why are we only looking at children in 6 states?

The funding for the study allowed us to support 6 study sites around the country.

Why are we only looking at children between the ages of 2-5?

The study will focus on children who are 2 to 5 years old. This age range was selected to reduce the amount of time since pregnancy and early development so that parent recall of events during these time periods is better, so that medical information is easier to retrieve, so that families are less likely to have moved away from the study area, and it will also be nearer the beginning of treatment for children in developmental intervention programs.

What is being investigated, and why?

* Physical and behavioral characteristics – Autism is a complex disorder and we want to better understand the full range of characteristics that are associated with autism. In this way, we may also better understand how the different causes of autism may be associated with specific subgroups of children within the autism spectrum.
* Infection and immune function, including autoimmunity – We want to follow up on reports that infections, or an abnormal response to infection – called the body’s immune response – may increase the risk for autism.
* Reproductive and hormonal features – We want to follow up on reports that abnormal hormone function – perhaps in the mother when she is trying to get pregnant, or later during pregnancy, or even later in the child after birth – may be associated with autism.
* Gastrointestinal features – We want to follow-up on reports that children with autism have abnormal gastrointestinal function, and whether it may be related to the causes of autism.
* Genetic features – Autism is a highly genetic disorder, but in particular we want to see if the genes that may be related to risk factors we are investigating – such as the genes that control immune function – are associated with autism.
* Socio-demographic features – We want to better understand the social, demographic, and economic features of families that are associated with having a child with autism.
* Smoking and alcohol use in pregnancy – Substance use in pregnancy can potentially harm the developing fetus and so we want to see if these so-called lifestyle factors are associated with autism.
* Sleep features – We want to follow-up on reports that children with autism have abnormal sleep patterns.
* Select mercury exposures – There are several studies, including studies funded by the government, looking at environmental exposures related to autism including mercury. CADDRE didn’t want to duplicate the work of these other studies, but we chose to look at information on vaccines and other types of medical procedures that may have mercury exposure that we can get through medical records.
* Occupational exposures – There are several studies, including studies funded by the government, looking at environmental exposures related to autism including mercury. CADDRE didn’t want to duplicate the work of these other studies, but we chose to ask parents to report to us about possible exposures they may have had at their jobs.

We selected these research factors after an extensive review of the literature. We designated each of the factors as high priority based on the how strongly they seemed to be associated with ASD and what new information we needed to collect about each factor, balanced by how well we could study each factor with our particular study methods.

What “selected mercury exposures” will be studied? How will they be studied? Why were these selected?

The mercury exposures we are looking at relate to vaccines or other medical treatments that are being studied include – vaccines that the mom received during pregnancy, the child’s vaccine exposures after birth and specific other factors such as RhoGAM treatment in pregnancy if the mom has developed an immune response against the fetus that can harm it.

There are several studies, including studies funded by the government, looking at environmental exposures related to autism including mercury. SEED didn’t want to duplicate the work of these other studies, but since we are getting medical records, we choose to look at information on vaccines and other types of medical procedures that may have mercury exposure that we can get through medical records.

Will the study include vaccines as a potential cause of autism?

Yes, the study will include vaccines. The mercury exposures being studies include – vaccines that the mom received during pregnancy, the child’s vaccine exposures after birth and specific other factors such as RhoGAM treatment in pregnancy if the mom has developed an immune response against the fetus that can harm it.

There are several studies, including studies funded by the government, now looking at environmental exposures in autism such as mercury. SEED doesn’t want to duplicate the work of these other studies, but since we are getting medical records, we choose to look at information on vaccines and other types of medical procedures that may have mercury exposure that we can get through medical records.

Will CDC find out if thimerosal causes autism?

It is too soon to speculate on the results of the study. We hope the study will give us a better idea of which of the risk factors that we will be looking at seem to be the most important in causing autism.

If the study shows that thimerosal is a cause of autism, will CDC report the data? What guarantees does the public have that the findings won’t be covered up?

We will report all the findings of the study by following the normal scientific review process as soon as possible.

When the study is completed, will we know the causes of autism?

It is too soon to speculate on the results of the study. We hope the study will give us a better idea of which of the risk factors that we will be looking at seem to be the most important in causing autism. The causes may be related to genes, the environment, or a relationship between the two – such as if some groups of children with certain genes are more easily harmed by some environmental exposures.

Will this study find a prevention/cure for autism?

It is too soon to speculate on what we might find about the causes of autism. But, we are hopeful that the findings from SEED will help the development of future studies specifically designed to assess treatments among children with autism.

What are the other developmental disabilities being studied?

We will be studying a range of other developmental disabilities, including mental retardation, developmental delay, and other behavioral problems in early childhood.

Why are we looking at other developmental disabilities?

By comparing children with autism and children with other developmental disabilities we will try to see if the risk factors we observe in children with autism are unique to autism or if they are also important in children with other developmental problems.

Looking at children with other developmental disabilities will also provide a way of comparing responses of children with developmental disabilities, in general, versus typically developing children.

How will you get the names of children to invite into the study?

We are working with our partners in the community who serve children with developmental problems and through these partners we will be sending out letters to families to invite them to participate.

Why didn’t or doesn’t the 2001/2002 funding represent “the first national study”?

In the initial grant awards (2001/2002), the grantees were responsible for 3 activities: setting up monitoring programs for autism and other developmental disorders, collaboration on the multi-site epidemiologic study, and investigator-initiated special studies. Although the multi-site study was planned, funding levels were not adequate to implement the multi-site study during the 2002/2002 funding cycle. Consequently, implementation was delayed until the current funding cycle. All funds awarded to the grantees in the current grant cycle are dedicated to implementation of the multi-site study. The grantees competed for funding to continue their monitoring activities under a separate grant announcement earlier in 2006, and no funding will be available for investigator-initiated special studies.

In what way(s) will the sample populations be representative of all children?

It seems that by not including major states like New York, Illinois, Texas, etc. it’s hard to claim this is “nationally representative”? Further, how will the selection/recruitment processes ensure or foster generalizability?

The two groups of children with ASD and other developmental problems will be identified in multiple clinical and educational facilities in each community to insure that the participants are representative of all children with these types of developmental problems – and not just children who might be seen at a single clinic or intervention program. The third group of study children will be randomly selected from all children born in each community during the same time period so that they are representative of all children in the study area most of whom do not have developmental problems.

Although resources do not permit the sample to be drawn so that it is statistically representative of all children in the nation, by conducting the study in 6 different geographic areas across the country with diverse populations and by identifying children from multiple sources in each community we hope to have a study sample that more closely represents children with ASD, other developmental problems, and typical development across the country.

Will there be interim results or will the study first have results six or so years from now?

Many of the core study hypotheses will require that we have data collection completed on the full study sample before analysis can take be completed, but some interim analyses that require less than the full study sample may be possible. We don’t want to rush interim analyses, however, before we have a good representative sample of children.

What do you mean by “community diversity”?

SEED is located in select study areas within 6 states: 2 counties in the San Francisco, California area, 7 counties in the Denver, Colorado area, 5 counties in the Atlanta, Georgia area, 7 counties in the Baltimore and northeast Maryland area, 10 counties in central North Carolina, and 3 counties in the Philadelphia, Pennsylvania area.

These study areas include diverse communities and populations from which study participants will be drawn.

Can this really be classified as a national study since it only involves six states?

It is a multi-site study set in diverse communities in 6 locations around the country: California, Colorado, Georgia, Maryland, North Carolina, and Pennsylvania.

Although resources do not permit the sample to be drawn so that it is statistically representative of all children in the nation, by conducting the study in 6 different geographic areas across the country with diverse populations and by identifying children from multiple sources in each community we hope to have a study sample that more closely represents children with ASD, other developmental problems, and typical development across the country.

How will this give us national insight?

Compared to a study located in a single area, our study in six different areas gives us geographic and community diversity that will give us greater insights into the variability of who is at risk and what are the risk factors for autism.

What is the methodology for collecting the data? Same for each state?

Yes, all the sites are using a common study protocol – meaning they are following the same procedures for recruiting participants and collecting data so that, at the end, the data from all 6 sites can be pooled into a single large data base for analysis.

We will be asking participants to complete self-administered questionnaires; interviewing mothers about pregnancy-related issues and developmental conditions in their children; conducting a developmental exam of each study child to evaluate cognitive and

emotional development, language and adaptive skills, and motor skills, and a dysmorphology exam of the child (that will look at physical features that may indicate an underlying genetic condition); taking cheek swab and blood samples from the mother; father, and child; taking a hair sample from the child; and looking at the mother and child’s medical records.

Do all 2,700 of the children have an ASD?

No, there will be 900 children in each of 3 groups: children with ASDs, children with other developmental problems, and children drawn from the community most of whom are typically developing.

I live in one of the states with a CADDRE center. Who can I contact for more information about the study?

California CADDRE
Kaiser Permanente Division of Research
California Department of Health Services
Oakland, CA
510.620.3700

Colorado CADDRE
Colorado Department of Public Health and Environment
University of Colorado at Denver and Heath Sciences Center
Denver, CO
303.315.0066
303.692.2680

Georgia CADDRE
National Center on Birth Defects and Developmental Disabilities
Atlanta, GA
404.498.3800

Maryland CADDRE
Johns Hopkins University
Kennedy Krieger Institute
Baltimore, MD
877.868.8014

North Carolina CADDRE
University of North Carolina at Chapel Hill
Chapel Hill, NC
919.966.2068

Pennsylvania CADDRE
University of Pennsylvania School of Nursing
The Children’s Hospital of Pennsylvania
Philadelphia, PA
215.573.2469
215.590.7474

Date: December 19, 2007
Content source: National Center on Birth Defects and Developmental Disabilities

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Nerve Cell Gene Linked to Autism
By Michael Smith, North American Correspondent, MedPage Today
Published: January 10, 2008
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston.

BALTIMORE, Jan. 10 — The risk for autism appears to increase in the presence of a common genetic variation on chromosome seven, especially when the condition is inherited from the mother, researchers here said.

The variant is a single nucleotide polymorphism (SNP) that’s found in 36% of the alleles of chromosome seven, according to Aravinda Chakravarti, Ph.D., of Johns Hopkins, and colleagues.

Dubbed rs7794745, the variant lies within a gene called contactin-associated protein-like 2 (CNTNAP2), Dr. Chakravarti and colleagues reported online in the American Journal of Human Genetics.

The gene, which encodes a protein involved in nervous system cellular interactions, had previously been associated with other neurological disorders, including cortical dysplasia-focal epilepsy and obsessive-compulsive disorder.

Also, two other papers in the journal reported links between autism and CNTNAP2. The reports come a day after researchers linked errors on chromosome 16 to the disorder. (See: Chromosome 16 Mutations Linked to Autism)

“CNTNAP2 is an excellent candidate gene for autism,” Dr. Chakravarti said.

“It encodes a protein that’s known to mediate interactions between brain cells and that appears to enable a crucial aspect of brain-cell development,” he added. “A gene variant that altered either of these activities could have significant impact.”

In a cohort of 72 families with multiple affected children — a total of 148 affected offspring and 292 other family members — the researchers performed a genome-wide scan for significant associations.

To reduce variation in the volunteers, the researchers required that the affected offspring meet a strict criterion of autism, rather than the broader “autism spectrum disorder.”

The gene scan found that a substitution of thymine for adenine at rs7794745 was significantly more common among those with autism (at P<2.14×10-5).

To confirm the finding, the researchers performed a separate genome-wide scan of 1,295 parent-child trios — this time with a broader definition of autism — and again found a significant over-transmission of the T allele (P<0.005) among the affected offspring.

Given the marked sex difference in autism — four times as many boys as girls are affected — the researchers also looked at which parent contributes the T allele to an autistic child.

The analysis found that the transmission frequency of the paternal T allele was 0.53 and the frequency of transmission of the maternal allele was 0.61, a difference that was significant at P<0.001, Dr. Chakravarti and colleagues said.

“This is a common variant,” Dr. Chakravarti said. “People inherit it all the time. Our finding that it’s associated with autism more often when it’s inherited from mothers is intriguing, but needs to be replicated.”

Meanwhile, using a language-based criterion — age at first word — another group of researchers found that a separate region of CNTNAP2 was associated with autism.

Daniel Geschwind, M.D., Ph.D., of the University of California at Los Angeles, and colleagues found that a SNP dubbed rs2710102 was significantly associated (P<0.028) with a delayed onset of speech.

In another study, researchers led by Matthew State, M.D., Ph.D., of Yale, found several rare variants in CNTNAP2 that appeared to be linked to autism.

Taken together, the three studies provide “unequivocal evidence” that disrupting CNTNAP2 leads to a subtype of autism spectrum disorder, said Dietrich Stephan, Ph.D., of the Translational Genomics Research Institute in Phoenix, in an accompanying commentary.

It’s now reasonable to say that people with autism combined with mutations in CNTNAP2 have “type 1 autism,” Dr. Stephan said.

The study was supported by the National Institute of Mental Health. Dr. Chakravarti did not report any potential conflicts.

Primary source: American Journal of Human Genetics
Source reference:
Arking DE, et al “A common genetic variant in the neurexin superfamily member CNTNAP2 increases familial risk of autism” Am J Hum Gen 2008; DOI: 10.1016/j.ajhg.2007.09.015.

Additional source: American Journal of Human Genetics
Source reference:
Stephan D, “Unraveling autism” Am J Hum Gen 2008; DOI: 10.1016/j.ajhg.2007.12.003.

Additional source: American Journal of Human Genetics
Source reference:
Alarcon M, et al “Linkage, association, and gene-expression analyses identify CNTNAP2 as an autism-susceptibility gene” Am J Hum Gen 2008; DOI: 10.1016/j.ajhg.2007.09.005.

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By Michael Smith, North American Correspondent, MedPage Today
Published: December 19, 2007
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine.

CAMBRIDGE, Mass., Dec. 19 — Altering just one gene allowed researchers here to correct many aspects of fragile X syndrome in mice.

• Fragile X syndrome is the most common heritable form of mental retardation and also the leading identified cause of autism.
• Add that loss of a single gene has been shown to be the basis of the syndrome, but the exact pathogenesis remains unclear.
• Note that this study, conducted in experimental mice, suggests that loss of the fragile X gene allows the product of a second gene to run amok, causing many of the symptoms of the syndrome.

The finding offers the possibility of therapy for the syndrome, which is the most common heritable form of mental retardation and the leading identified cause of autism, according to Mark Bear, Ph.D., of the Massachusetts Institute of Technology, and colleagues.

The loss of the gene for fragile X mental retardation protein (FMRP) is known to cause the syndrome, but it hasn’t been clear exactly how, Dr. Bear and colleagues said in the Dec. 20 issue of Neuron.

A series of experiments in mice that lack the equivalent of the fragile X gene appear to show that FMRP acts as a brake on a second protein, a metabotropic glutamate receptor dubbed mGluR5, the researchers said.

Reapplying the brake by reducing the expression of mGluR5 prevented aspects of the syndrome, the researchers said, including a tendency to seizures, altered body growth, and a different pattern of brain structure and function.

The “constellation of findings,” the researchers concluded, implies that “fragile X is a disorder of excess … and these excesses can be corrected by reducing mGluR5.”

Dr. Bear and colleagues experimented with four lineages of mice — wild-type mice, mice lacking FMRP but not mGluR5, mice with FMRP but lacking one of the two mGluR5 alleles, and mice without FMRP and lacking one of the two mGluR5 alleles.

Missing one of the mGluR5 alleles reduced expression of the protein by 50%, the researchers said.

The animals lacking FMRP but with fully functioning mGluR5 (dubbed KO mice) exhibited many of the aspects of fragile X seen in humans with the condition, while those without FMRP but with a lowered expression of mGluR5 (dubbed CR mice) were similar to wild-type.

For example, an increased density of dendritic spines on neurons, the major targets of excitatory synapses in the brain, is associated with fragile X in humans.

Similar abnormal neurons were seen in the KO mice, the researchers said, but not in the CR animals.

The KO mice — whose wild-type ancestors are resistant to seizures — have a tendency to epilepsy-like convulsions in response to certain tones, which is a consequence of the loss of FMRP, the researchers said.

In this study, 72% of the KO animals seized when exposed to the tone, compared with none of the wild-type mice, a difference that was significant at P<0.0001. But the tendency to seizure was significantly attenuated (P=0.028) in the CR mice, the researchers said.

Humans with fragile X show accelerated prepubescent growth and the KO mice also showed a 10% increase in average weight within a few days of weaning, compared with wild-type and CR animals. The differences were significant at P=0.017 and P=0.004, respectively.

The data show “unambiguously” that the two proteins oppose each other, the researchers concluded, and support the idea that many aspects of fragile X are the result of unopposed activation of mGluR5.

Macro-orchidism is also a feature of the fragile X syndrome, however, there was no evidence of an interaction between FMRP and mGluR5 in the control of testicle size in the mice.

Primary source: Neuron
Source reference: Dölen G, et al “Correction of fragile X syndrome in mice” Neuron 2007; 56: 955-62.

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And this will seem to explain why for some its a stomach and diet issue, for others cellular and for still others more cerebral symptoms.

Again, another connection to Meditating and insight form the Dali Lama.
Story By Jamie Talan.
It used to be dogma that the brain was shut away from the actions of the immune system, shielded from the outside forces of nature. But
that’s not how it is at all. In fact, thanks to the scientific detective work of Kevin Tracey, MD, it turns out that the brain talks
directly to the immune system, sending commands that control the body’s inflammatory response to infection and autoimmune diseases.
Understanding the intimate relationship is leading to a novel way to treat diseases triggered by a dangerous inflammatory response.
Dr. Tracey, director and chief executive of The Feinstein Institute for Medical Research, will be giving the 2007 Stetten
Lecture on Wednesday, Oct. 24, at the National Institutes of Health in Bethesda, MD. His talk – Physiology and Immunology of the Cholinergic
Anti-inflammatory Pathway – will highlight the discoveries made in his laboratory and the clinical trials underway to test the theory that
stimulation of the vagus nerve could block a rogue inflammatory response and treat a number of diseases, including life-threatening
sepsis.
With this new understanding of the vagus nerve’s role in regulating inflammation, scientists believe that they can tap into the
body’s natural healing defenses and calm the sepsis storm before it wipes out its victims.
Each year, 750,000 people in the United States develop severe sepsis, and 215,000 will die no matter how hard doctors fight to save them.
Sepsis is triggered by the body’s own overpowering immune response to a systemic infection, and hospitals are the battlegrounds for these
potentially lethal conditions.
The vagus nerve is located in the brainstem and snakes down from the brain to the heart and on through to the abdomen. Dr. Tracey and
others are now studying ways of altering the brain’s response or targeting the immune system itself as a way to control diseases.
Dr. Tracey is a neurosurgeon who came into research through the back door of the operating room. More than two decades ago, he was
treating a young girl whose body had been accidentally scorched by boiling water and she was fighting for her life to overcome sepsis. She didn’t make it.

Dr. Tracey headed into the laboratory to figure out why the body makes its own cells that can do fatal damage. Dr. Tracey discovered that the
vagus nerve speaks directly to the immune system through a neurochemical called acetylcholine. And stimulating the vagus nerve
sent commands to the immune system to stop pumping out toxic inflammatory markers. “This was so surprising to us,” said Dr. Tracey,
who immediately saw the potential to use vagus stimulation as a way to shut off abnormal immune system responses.
He calls this network “the inflammatory reflex.” Research is now underway to see whether tweaking the brain’s acetylcholine system could be a natural way to control the inflammatory response. Inflammation is key to many diseases – from autoimmune conditions like Crohn’s disease and rheumatoid arthritis to Alzheimer’s, where scientists have identified a strong inflammatory component.
Dr. Tracey has presented his work to the Dalai Lama, who has shown a great interest in the neurosciences and the mind-body
connection. He has also written a book called “Fatal Sequence,” about the double-edge sword of the immune system.

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CINCINNATI, Sept. 4 — Almost 9% of U.S. children ages 8 to 15 meet standard diagnostic criteria for attention-deficit/hyperactivity disorder (ADHD), but less than half of them receive treatment. Action Points * Explain to interested parents that this study suggests that less than half of the 2.4 million children ages 8 to 15 who meet standard diagnostic criteria for ADHD receive treatment. * Note that there are also ADHD prevalence discrepancies between racial and ethnic groups and according to socioeconomic status. Only 47.9% of the 2.4 million who met Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for ADHD had reportedly had their conditions diagnosed by a health care professional or been treated with medication, according to a report in the September issue of the Archives of Pediatrics & Adolescent Medicine.

A research team led by Tanya E. Froehlich, M.D., of Cincinnati Children’s Hospital Medical Center did a cross-sectional phone survey of the parents or caregivers of 3,082 eight- to 15-year old children who were participants in the National Health and Nutrition Examination Survey. Survey respondents provided information about each child’s ADHD symptoms between 2001 and 2004. They also provided sociodemographic information and information about whether the child had ever been diagnosed with ADHD or taken medicine to treat the disorder.

The researchers found that 8.7% (95% CI; 7.3%-10.1%) met the DSM-IV criteria for ADHD in the year before the survey took place. An additional 3.3% of children did not meet the criteria, but had a parent-reported prior diagnosis and had been treated with an ADHD medication at some point during the previous year. The latter group, however, was not included in the main analysis. More boys than girls met the diagnostic criteria for ADHD, 11.8% versus 5.4%, respectively (P<0.001), but girls were less likely than boys to have had the disorder recognized. There were also discrepancies in ADHD rates by race and ethnicity. Non-Hispanic white children were more likely to meet criteria for ADHD than were Mexican-American children or children of other races/ethnicities, the study showed. These findings held in both bivariate and multivariate analyses.

The study authors could not explain why Mexican-American children had lower rates of ADHD, but they speculate that this may be related to “differences in the prevalence of causal risk factors, genetic susceptibility, and/or rates of reporting ADHD symptoms across cultures.” Of the children who met the diagnostic criteria for ADHD, 38.8% had received medication to treat inattention, hyperactivity, or overactivity in the prior year and 32.0% had been taking medication for most of that year. Regular medication use was more likely to be reported for older children than younger ones, the study showed. Money also mattered in the new study. Children in the poorest quintile were more likely than those in the wealthiest quintile to have been diagnosed with ADHD (adjusted odds ratio [AOR] for PIR, first quintile vs fifth quintile, 2.3; 95% CI, 1.4-3.9). “Reasons for the increased likelihood of ADHD in poorer children may include the elevated prevalence of ADHD risk factors (i.e., premature birth and in utero or childhood exposures to toxic substances) in this group,” the study authors write. “In addition, given the high heritability of ADHD and its negative impact on social, academic and career outcomes, it is plausible that families with ADHD may cluster within the lower socioeconomic strata.” Although poor children were more likely to have ADHD, the poorest children were three to five times less likely to consistently receive medication when compared with their counterparts in other income groups, the researchers noted.

This finding “warrants further investigation and possible intervention to ensure that all children with ADHD have equitable access to treatment when appropriate,” the authors conclude.

The researchers also analyzed ADHD by subtypes. Specifically, 4.4% of the children met the criteria for ADHD-1A, 2.2% for ADHD-CT and 3.0% for ADHD-HI. The poorest children were more likely to have ADHD-HI than their wealthier counterparts (AOR for PIR, first vs fifth quintile, 3.1; 95% CI, 1.2-8.3). In addition, African Americans and Mexican Americans were less likely to have ADHD-1A, compared to their non-Hispanic white counterparts, the study showed. None of the study authors reported any financial conflicts.

The study was funded by an Ambulatory Pediatrics Association Young Investigator Grant, a National Research Service Award grant, and grants from the NIH and Robert Wood Johnson Foundation. Additional ADHD/ADD Coverage Additional source: Archives of Pediatrics & Adolescent Medicine Source reference: Froehlich TE, “Prevalence, Recognition, and Treatment of Attention-Deficit/Hyperactivity Disorder in a National Sample of US Children” Arch Pediatr Adolesc Med. 2007; 161(9): 857-864.

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By Charles Bankhead, Staff Writer, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
August 30, 2007
add your knowledge 1 Add Your Knowledge™ Post     Additional Autism Coverage

BRISTOL, England, Aug. 30 — Autistic children have an impaired ability to place unfamiliar faces in memory, possibly explaining some of the social difficulties associated with the disorder, investigators here concluded.

Keep In Mind

* This study shows that children with autism appear to have a reduced ability to adapt mentally to faces that differ substantially from familiar faces.

* This study suggests that reduced facial recognition abilities might be related to social problems associated with autism.

* Note that the findings are based on a small number of patients.

Specifically, children with autism have difficulty with face identity aftereffect, the ability to fix in memory faces that are polar opposites of familiar faces, Elizabeth Pellicano, Ph.D., of the University of Bristol, and colleagues, reported online and in the September issue of Current Biology.

The human brain seemingly has the ability to encode new faces in a “face space,” Dr. Pellicano explained. Average or typical faces are in the center of the space. More distinctive faces lie toward the periphery, making them easier to distinguish from faces that are closer to average.

In people with normal face recognition abilities, she continued, the brain automatically places a new face in the face space on the basis of deviations from the average.

“The really neat bit is that the precise characteristics of what constitutes an average face are continuously updated based on our experiences in looking at other people,” said Dr. Pellicano.

In the current study, the face identity aftereffect capabilities of 14 high-functioning boys with autism spectrum disorder were compared with those of 15 age- and ability-matched nonautistic boys (mean age about 11 years in both groups).

Scores on standardized tests showed the two groups had similar verbal and nonverbal abilities, but they differed significantly on the Social Communication Questionnaire (P<0.001).

The study participants were introduced to the faces of “Dan” and “Jim,” who were described as “team captains.” The boys then viewed computer-generated faces that resembled Dan or Jim to varying degrees. The two groups of boys demonstrated similar ability to place the new faces on Dan’s or Jim’s team.

The boys then viewed computer-generated faces that had features that were opposite those of Dan or Jim. After viewing these distinctly different faces, the normal boys substantially improved their ability to place faces that resembled Dan or Jim on the correct team. In contrast, the autistic boys showed little improvement in their aftereffect abilities (P<0.05 versus the normal group).

In the group of autistic boys, aftereffect scores had a significant correlation with Social Communication Questionnaire scores (r= -0.60, P<0.05). For the typically developing boys no significant correlation existed between aftereffect and the communication scores.

Dr. Pellicano and colleagues examined a subgroup of nine autistic boys with high social communication scores associated with more symptoms related to socialization, communication, and restrictive/repetitive interests. The boys’ aftereffect was about one-third that of the typically developing boys (P<0.01).

Because the normal and autistic groups demonstrated similar precision for recognizing Dan-like and Jim-like faces, the investigators ruled out poor identification performance or task motivation as the cause of reduced aftereffect in the boys with autism. Moreover, the boys inspected the faces with a similar degree of intensity.

“Reduced attention to the adapting faces could potentially contribute to the weaker aftereffect in autism, and we see the relationship between adaptation and attention as a promising direction for future research,” the authors stated.

Although face-reading difficulties might contribute to the social problems characteristic of autism, an early lack of interest in social phenomena could contribute to development of atypical face-coding mechanisms, they added.

The authors had no disclosures. The study was supported by the Australian Research Council and the Experimental Psychology Society of England.
Additional Autism Coverage

Primary source: Current Biology
Source reference:
Pellicano E et al. “Abnormal adaptive face-coding mechanisms in children with autism spectrum disorder.” Curr Biol 2007; 17: 1508-1512.

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I have to tell you, I’ve been skeptical of plastic for the past 5 years and 9 months. I often look at what was around when I was a kid versus today and it comes down to cell phones, computers and plastic everything. I never drank from a plastic cup as a child and today kids barely know what a glass is. And who knows how many plastic bottles of Poland Spring or Gatorade I have consumed this week alone, let alone the past 15 years or so.

Ask a vet and they will tell you, feed your pet from stainless steel or glass as plastic harbors germs and will cause a rash around the pets mouth. If you ever have had a pet with this problem, you know a switch to a stainless steel or glass bowl and shazaam, the rash disappears rather quickly. So why is it different for humans? Simple, lobbyists who fight for company’s such as DuPont and Union Carbide, who have been poisoning the people of this planet for decades to just make another buck of profit.

Although this report shows there is reason for some concern with BPA to Human Development, it downplays the connection. It should also be noted that the study is based only upon oral contact with the chemical, injections are a much better measure of how it would affect an unborn fetus. Here is a link to the study..

Plastics Chemical of ‘Some Concern’ for Fetal, Child Health
08.08.07, 12:00 AM ET

WEDNESDAY, August 8 (HealthDay News) — Bisphenol A, a chemical found in many plastics and resins, may present some risk to a developing fetus and children, a U.S. government panel concluded Wednesday.

Experts convened by the U.S. Center for the Evaluation of Risks to Human Reproduction (CERHR), part of the National Toxicology Program, unanimously concluded that exposure to bisphenol A (BPA) presents some risk to human development and reproduction.

BPA is chemical used in the production of polycarbonate plastic and several types of resins. It is found in products used everyday such as compact discs, DVDs, baby bottles and other food and drink packaging. It is also commonly found in cars, sports safety equipment and water pipes.

“The panel’s finding means that we cannot dismiss the fact that exposure to this substance may be causing effects on reproductive health,” CERHR Director Michael D. Shelby said.

However, “It’s going to take more research to verify what those effects are,” he said.

Animal experiments have suggested that BPA may mimic the female sex hormone estradiol. The fear has been that exposure to BPA can cause birth defects and developmental problems.

In addition, exposure to BPA has been blamed for a variety of other problems, including cancer, diabetes, obesity and attention deficit disorder.

Exposure to BPA can occur through direct contact or by exposure to food or drink that has been in contact with material containing BPA.

“The conclusions of the expert panel are expressed in levels of concern,” Shelby explained. The lowest level is “negligible concern,” followed by “minimal concern,” then “some concern,” “concern” and then “serious concern,” he said.

The panel found “some concern” that exposure to BPA causes neural and behavioral effects to the fetus. The panel members expressed “minimal concern” that exposure to BPA causes effects to the fetal prostate or that exposure causes an acceleration of puberty, Shelby said.

The panel also said there was “negligible concern” that the chemical causes birth defects and malformations.

However, the panel expressed “some concern” that BPA exposure causes neural and behavioral effects in children, Shelby said. It also said it had “minimal concern” that BPA would cause children to experience accelerations in puberty.

For adults, the panel found “negligible concern” that there would be adverse reproductive effects following exposure to BPA. In addition, it had “minimal concern” for people exposed to BPA at work, Shelby said.

The panel did recommend that studies be done that would remove the uncertainties in some of its conclusions, or raise or lower the level of concern it had expressed, based on the data available, Shelby said.

The committee’s report is not without its critics.

“If I were a committee member, I wouldn’t sign off on this broken report,” said Jennifer Sass, senior scientist for the Health and Environment Program at the Natural Resources Defense Council, an advocacy group.

“Harmful effects in laboratory animals exposed to even the low levels of BPA that are commonly found in the blood and urine of Americans include an increase in prostate and breast cancer, type 2 diabetes, reproductive abnormalities, reduced semen quality, recurrent miscarriage, obesity, and neurobehavioral problems similar to attention deficit hyperactivity disorder,” she said in a prepared statement.

The biggest problem with the report is the decision to limit the review to oral-dose studies, primarily the industry-sponsored studies, and not injection studies, the council said.

“This means they failed to include evidentiary science of the full range of risks to unborn fetuses, who receive BPA through the contaminated blood circulation, irrespective of the pregnant mothers route of exposure,” the group stated.

Reports from the National Toxicology Program are used by state and federal regulators to establish exposure standards, and are a resource for regulatory agencies to allocate resources toward most effective strategies to protect human health, the council noted.

A chemical industry representative took another view.

“What we saw today was a triumph of solid science,” said Steven Hentges, executive director of the Polycarbonate/BPA Global Group of the American Chemistry Council, which represents chemical manufacturers. “The panel of experts came up with what is really a very reassuring conclusion on the safety of BPA,” he said.

Hentges believes more research is needed in areas where the panel found “some concern.”

“Based on the science we do not think that additional regulation is needed,” he said. “The products in use today are safe.”

More information

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COLD SPRING HARBOR, N.Y., July 26 – Autism, a developmental disorder, may more likely be carried by mothers and dependent on parental age, according to U.S. researchers.

Researchers at Cold Spring Harbor Laboratory and Albert Einstein College of Medicine analyzing the incidence of autism found a previously unrecognized pattern pointing to a spontaneous germ-line mutation model of disease acquisition.

The study, published in the Proceedings of the National Academy of Sciences, indicates parents, especially women — who acquire the mutation but do not exhibit severe symptoms of the disorder — have a 50 percent chance of passing the mutation on to their children. Sons often show the most severe symptoms.

“The fact that germ-line mutations increase with age places older parents at a higher risk of having children with autism, explaining a pattern that has been recently observed,” study co-author Michael Wigler, of CSHL, said in a statement.

The model proposes two risk classes. One is sporadic or low risk autism — the more common form — caused by spontaneous germ-line mutation. The children, mostly female, who receive such a mutation but do not display the disorder, are the source of the other risk class — high risk families. Boys in high risk families may account for a quarter of autism. according to the study.

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To understand the meaning of a conversation, kids automatically do what adults do – besides processing the meaning of words, they unconsciously ‘read’ the expression on a person’s face and listen to their tone of voice, then integrate that information with the context at hand to discern meaning, be it humor, anger, irony or straightforwardness.

Individuals with autism typically don’t do this. They often miss the subtle meanings conveyed by a person’s face and tone of voice, and thus have trouble determining the communicative intent of others. Neuroimaging studies have backed this up, showing that individuals with autism spectrum disorders (ASDs) – including autism, pervasive developmental disorder and Asperger’s syndrome – show reduced activity in the regions of the brain that respond to such cues.

But what if those brain regions could be trained to respond appropriately” In a report in the current issue of the journal Archives of General Psychiatry and currently online, UCLA researchers did just that. Providing ASD children with explicit instructions to pay more attention to facial expressions and tone of voice elicited an increased response in the medial prefrontal cortex, part of the brain’s network for understanding the intentions of others.

“That’s significant. The fact that you can ‘normalize’ activity in this region in the ASD group by directing their attention to these important social cues clearly indicates there’s nothing intrinsically wrong with this region in the autistic brain,” said Mirella Dapretto, associate professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA and a member of the UCLA Ahmanson-Lovelace Brain Mapping Center. Dapretto co-authored the study with her former graduate student Ting Wang, who is now a postdoctoral fellow at Mount Sinai School of Medicine.

“This is a very positive thing,” Dapretto said, “because these findings have implications for future interventions” they suggest that you could train the autistic brain to make use of the information conveyed by the human face and voice to successfully navigate social interactions

Autism is a complex neurobiological disorder of development that affects one of every 150 children, impairing communication and social skills. ASDs encompass a broad spectrum of disorders that range from mild to severe.

The authors had two goals in mind with their study. One was to examine the neural circuitry in the brain that underlies the problems ASD children face in interpreting communicative intent. The other was to determine whether explicit instructions to pay attention to facial expressions and tone of voice would elicit more normal patterns of brain activity in these children.

While undergoing functional magnetic resonance imaging (fMRI), 18 ASD boys between the ages of 7 and 17, as well as a control group of 18 typically developing (TD) boys, viewed cartoon drawings of children in conversational settings while listening to short vignettes that ended with a potentially ironic remark. Researchers found that, compared with the TD control group, the ASD children had reduced activity in two areas of the brain – the medial prefrontal cortex and right superior temporal gyrus. But when the researchers gave both groups explicit instructions to pay attention to the speaker’s facial expression and tone of voice, only the ASD children showed a significant increase in activity in the medial prefrontal cortex.

“The typically developing kids recognized and interpreted these cues automatically when trying to infer if a speaker’s remark was sincere or sarcastic, so their brains were already responding appropriately,” said Dapretto. “But not so with the ASD kids, who did not show activity in this area when specific instructions weren’t provided. This is the first study to show that you can normalize activity in a key region of the so-called ‘social brain’ in individuals with autism by simply directing their attention to these important social cues.”

—————————-
Article adapted by Medical News Today from original press release.
—————————-

Other authors of the study included Susan S. Lee and Marian Sigman. The research was funded by the National Alliance for Autism Research, the Cure Autism Now Foundation, the UC Davis M.I.N.D. Institute, and grants from the National Institute of Child Health and Human Development and the National Institute on Deafness and Other Communication Disorders.

The Semel Institute for Neuroscience and Human Behavior at UCLA is an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior and the causes and consequences of neuropsychiatric disorders. In addition to conducting fundamental research, the institute faculty seeks to develop effective treatments for neurological and psychiatric disorders, improve access to mental health services and shape national health policy regarding neuropsychiatric disorders.

Contact: Mark Wheeler
University of California – Los Angeles

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Next time you lose your car keys and enlist the family to help you search, try a little experiment. After your spouse searches an area, go and look in the same place. It will likely feel strange, even irritating to both of you – and that’s because you may be fighting an ancient, hard-wired, human behaviour pattern.

The behavioural phenomenon is called ‘inhibition of return’ and for our ancient hunter-gatherer ancestors it made a lot of sense. As Dr. Tim Welsh explains, “This behaviour likely developed through evolution to increase search efficiency. Returning to search an area that someone else has already searched doesn’t make a lot of sense from a survival point of view because they’ve either found the food and eaten it, or there’s no food there.”

Inhibition of return has been well-documented over the years, but Welsh is interested in measuring exactly how the actions of another individual affect our own, and whether people with autism react differently than the rest of the population. To test this Welsh, a professor in the Faculties of Kinesiology and Medicine, came up with a unique and elegant experiment that uses some cutting-edge technology.

In Welsh’s set-up, two subjects sit across from each other wearing, liquid crystal goggles. They are told to reach for a lighted target in front of them.

Welsh’s previous work has shown that if we see someone else touching an area, we are much slower to move there, but Welsh wanted to see how much of another person’s actions we need to be aware of, to affect our own. Welsh’s crystal goggles become opaque allowing the subject to see only a fraction of the other person’s movement.

He discovered that as social beings, we are so sensitive to another’s actions that just the suggestion of a movement was enough to trigger the inhibition of return effect.

So what happens when the individual doesn’t really recognize, or can’t recognize the actions of another individual” Sadly this is often the case for people with autism, a complex neurological, developmental disability that affects over 50,000 Canadians. A current theory of autism is that individuals with the disorder have a problem with their mirror neuron system.

“In normal individuals if you see someone throwing a ball, your mind will ‘mirror’ those actions to make it seem as if you are throwing it yourself,” Welsh explains. “The theory is that a person with autism may not be able to mirror the actions of other individuals. So in our experimental set-up you would expect them to be unaffected by the actions of another person and this is exactly what we have found to this point.”

Welsh believes his research will advance our understanding of autism and the mirror neuron system – perhaps leading to more effective intervention and treatment of a condition that seems to be growing at an alarming rate. “What I think is very interesting,” says Welsh, “is that the same experimental set-up can effectively be used to test two theories, and in many ways the two groups we are working with – a typically-developing population and an autistic population – provide a control for the other group. I’m very excited about this research.”

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Article adapted by Medical News Today from original press release.
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Dr. Welsh is currently looking for people between the ages of 14 and 25 to participate in his experiments. He is looking for with people autism and people from the typically-developing population.

Contact: Don McSwiney
University of Calgary

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NEW HAVEN, Conn., June 8 (UPI) — U.S. researchers have identified a new regulatory target for the Fragile X mental retardation protein, laying the groundwork for possible new treatments.

Fragile X syndrome, or FXS, is the leading inherited form of mental retardation.

The findings, published in the early online edition of the Proceedings of the National Academy of Sciences, also have implications for autism, which shares a common physiological pathway with FXS, according to researchers at the Yale School of Medicine.

The research team, led by Dr. Yingqun Huang, previously found that FMRP — a protein without which brain development is hampered and nerve cells cannot communicate with each other — interacts with nuclear mRNA export protein NXF2 in the mouse brain and testes.

“Our findings explain why the NXF1 protein level is much lower in the hippocampal — brain — neurons involved in learning and memory than in many other cells,” Huang said in a statement.

“This may suggest that a high level of NXF1 might hinder the function of these cells.”

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We have often thought about the link between technology and Autism’s rise. Computers and cellphones, their growth and prevalence mirrors that of Autism diagnosis. This is the first of hopefully more looks into this area.

       A new report is claiming to have found a link between the rise in autism in the USA, and the rise of the use of wireless technologies,specifically mobile phones. Tamara Mariea, founder of Internal Balance, is releasing findings from more than five years of research on clients with autism, and other membrane sensitivity disorders which claims electromagnetic radiation stress is one of the potentially major root causes of the explosion of autistic cases in the past two decades.

      People who visit the Internal Balance clinic are “detoxed” in an electromagnetic radiation clean environment.

In simple terms, Mariea explains to parents struggling to help their children that what her research is pointing to is with more cell phone towers being erected, more cell phones in use globally and more WiFi technology utilized, the risk for autism continues to rise. She says that Thimerosal – the mercury containing preservative in scheduled children’s  vaccines – has for the most part been eliminated from regularly scheduled childhood vaccines, according to public record and that the incidence of autism should be decreasing based on progress made in that area in recent years. But, it is not decreasing, she says. This is where Mariea and Dr. Carlo began to collaborate in the search to find what the larger contributor to the increase in autism is.

      They say that the epidemiologic curve of autism parallels too closely with the increase usage of wireless devices to not look at it. Mariea’s soon to be published paper will include her research which explores electromagnetic radiation as a cohort effect with heavy metals as a strong component of the etiology of autism.

      We shall have to wait and see if the report has any credible findings when it is published.

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MILTON, Ontario, Feb. 19 — Genes associated with an autism risk appear to be clustered in a region on chromosome 11, according to the largest study yet of families with a predisposition to the condition.
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In a study of more than 1,100 families, the Autism Genome Project Consortium, consisting of 137 investigators from 50 centers in 19 countries, has closed in on a stretch of the chromosome where genes involved with the neurotransmitter glutamate are known to lie, reported Peter Szatman, Ph.D., of McMaster University, Bernie Devlin, Ph.D., of the University of Pittsburgh, and colleagues, online in Nature Genetics.

“This study is by far the largest study ever conducted, in terms of both researchers and research subjects,” said Joachim Hallmayer, M.D., of Stanford, a co-author. The results point the way toward further studies, but are far from definitive, the authors acknowledged.

“While promising, these results need to be followed up with more refined genetic maps to home in on other specific candidate genes. We also need to look more closely at chromosomal anomalies in large samples of children with autism,” Dr. Hallmayer said.

The investigators conducted genetic analyses on 1,168 families in which two or more members had a diagnosis of autism, as defined by either the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule, or by clinical evaluation.

Genetic analysis of such a large sample may be particularly revealing the authors wrote, because autism has a strong genetic component. They pointed out that in twin studies, there is a concordance for autism of 60% to 92% among identical (monozygotic) twins, and up to 10% for dizygotic pairs.

“Although familial clustering in autism could reflect shared environmental factors, twin studies and the distribution of milder phenotypes in families favors a model involving multiple interacting loci,” the investigators wrote.

They hypothesized that autism is a joint or combined genetic affair in which various combinations of susceptibility alleles may play a role.

They used automated genotype analysis techniques to conduct genetic linkage analysis, which looked for specific genetic markers in the vicinity of a suspected autism susceptibility gene.

They also tracked chromosomal abnormalities among affected family members by looking at copy number variations, sub-microscopic genomic insertions, and deletions implicated in various disorders, including autism.

“Although we know autism is highly heritable, complex gene interactions and submicroscopic anomalies create a din of statistical noise that drowns out detection of signals from linked sites in the genome,” said Dr. Devlin. “To amplify these signals, we brought to bear gene chip technology with a huge sample, and also screened for these fine-level anomalies, factoring them into the analysis.”

There is also evidence that chromosomal abnormalities or genetic disorders such as fragile X syndrome or tuberous sclerosis syndrome, both of which involve aberrant glutamate signaling, may be involved in autism risk, they wrote.

Using the genetic linkage analysis, the authors found that the 11p12-p13 region of chromosome 11 was most closely linked to neuroligins, transmembrane proteins expressed on the postsynaptic cell that bind to presynaptic transmembrane proteins called β-neurexins.

The candidate genes are involved in the trans-synaptic transportation of glutamate, a major excitatory neurotransmitter.

“We also found a family with a deletion in a gene called neurexin 1 that appeared to correlate with a diagnosis of autism in this family,” Dr. Hallmayer said.

Two young girls in the family with the neurexin 1 deletion presented with typical autism, including characteristic developmental delays; one child appeared to be nonverbal, and that other had mild language regression.

Neurexin 1 encodes for a protein that facilitates interneuronal communication. Deficits or defects in glutamate function have been implicated previously in autism and other neurodevelopmental disorders.

“As for the chromosome 11 location, we think there is another susceptibility gene there and we are actively pursuing it,” said co-author Gerad Schellenberg, Ph.D., of the University of Washington in Seattle. “We are in the neighborhood and have a plan to find it.”

The study was funded by the non-profit organization Autism Speaks and by the National Institutes of Health. The authors disclosed no financial conflicts.

Primary source: Nature Genetics
Source reference: Szatmari P et al. “Mapping autism risk loci using genetic linkage and chromosomal rearrangements.” Nature Genetics doi:10.1038/ng1985

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By Michael Smith, Senior Staff Writer, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
February 09, 2007

EDINBURGH, Scotland, Feb. 9 — Rett syndrome — a relatively rare autism spectrum disorder — may be reversible, if experiments in mice are borne out in humans.

The syndrome, which affects about one in 10,000 girls, is caused by mosaic expression of mutations in the X-linked gene MECP2 and destroys speech, normal movement, and use of the hands, although there is no loss of neurons, according to Adrian Bird, Ph.D., of the University of Edinburgh.

But in a mouse model of the syndrome, symptoms could be reversed completely, even in animals that were severely affected, Dr. Bird and colleagues reported online in the Feb. 9 issue of Science.

“The general perception in the field is that once you have damage in the brain, it’s very difficult to go backwards,” Dr. Bird said. “What we found is that (Rett syndrome is) reversible.”

The finding is both the “most desirable (and) the most unexpected result” of the experiments, Dr. Bird said in a statement.

Huda Zoghbi, M.D., of Baylor College of Medicine in Houston — who discovered that the syndrome is caused by MECP2 mutations — called the findings “extraordinary.”

And, since MECP2 mutations are now being seen in some cases of childhood schizophrenia, classic autism and learning disabilities, the results may have a wider application than just to Rett syndrome, she said.

“If we can develop therapies to address the loss of MECP2 we may be able to reverse neurological damage in children and adults with Rett, autism and related neuropsychiatric disorders,” said Dr. Zoghbi, who was not involved with the Edinburgh research.

However, the researchers cautioned that the “experiments do not suggest an immediate therapeutic approach” to Rett syndrome.

Dr. Bird and colleagues made the discovery using genetically engineered mice, whose MECP2 gene was silenced by a so-called stop cassette. The silencing could be reversed at will by administering the estrogen analog tamoxifen.

The researchers measured symptoms in the mice with observational tests for such things as gait, tremor, irregular breathing, and poor ability to clasp with the hind limbs. A wild-type mouse would score zero for all symptoms, while mice with the syndrome would score one if a symptom was present and two if it was severe.

The key experiment, Dr. Bird and colleagues said, was in female mice that had developed symptoms:

* Wild-type littermates had no symptoms, as expected.
* Untreated experimental animals had symptom scores averaging above four.
* Mice treated with tamoxifen over a four-week period (thus slowly reactivating their MECP2 gene) saw their symptom scores progressively reduced, to one or below.
* The difference in symptom scores between the two groups of experimental mice was significant at P<0.002.

The researchers also measured neuronal signaling in the mice, and particularly long-term potentiation (LTP), which is thought to be the cellular basis for learning and memory.

In female experimental mice, the onset of symptoms coincided with a reduction in LTP, compared with wild-type mice, the researchers found. However, after treatment to restore the gene function, LTP in the experimental mice was indistinguishable from wild-type.

“Like many other people, we expected that giving MECP2 to mice that were already sick would not work,” Dr. Bird said. “The idea that you could put back an essential component after the damage to the brain is done and recover an apparently normal mouse seemed farfetched.”

Yet, he added, “the results are gratifyingly clear, and must give hope to those who are affected by this distressing disorder.”

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