Unlock Autism

For the past year or so, I have tried to watch every movie with an Autism link in it in hopes of learning or as a source of inspiration. And for the most part, this has worked in providing insight and further understanding. Recently, I watched the Temple Grandin movie starring Claire Danes on HBO last night. All I can say is very well done and impressive. I highly suggest making time to view this movie which to me was dead on.

Here is a speech given by Temple Grandin that is sure to educate and inspire. Here are some insights from Temple on what to do as soon as you know or see an indication of Autism. “When I was a little kid, I had all the symptoms – no speech and really severe autism,” she says. “You’ve gotta work with the kids really young … My mother made sure I had my first job when I was 13, working for a seamstress. When I was in college, I had internships at a research lab and at a school for autistic kids.” Early intervention is key.

There are a wealth of great tips and insights in this video for anyone who is in contact with an autistic person- Focus on strengths, Don’t punish sensory issues, The Autistic brain is highly detailed and constantly at work, limit surprises. Thinking in pictures- a mind that works like Google search engine for images and more…

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• Temple Grandin’s theories on autism (marginalrevolution.com)
• Temple Grandin premieres on HBO (timeoutny.com)
• Claire Danes as the Autistic Temple Grandin (cinematical.com)
• Claire Danes plays autistic icon Temple Grandin (trueslant.com)
• Autism through a time machine (thestar.com)

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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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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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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.”

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

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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There was an interesting article in the last “Weekend Journal” (Jan 19-21) The question put forward by the Dalai Lama -could a person change the physical nature of the brain through mediation? Most doctors said no at first but then tests soon began. Researchers were able to give credence to the idea that the physical of the brain could be changed through meditation. They used a brain scan to show that a person who meditated was able to relax their thought producing frontal lobes and in fact medications such as Paxil taken for anxiety actually increased brain activity in the frontal lobes of the brain and decreased activity in the feel good rear of our brains.
(I will get this link and update this post) I thought, the same procedure could be used to look at how an Autistic brain functioned, surely we have tried this? After a few minutes of meditation , I was able to relax. Then I find this article.

By Mark Roth, Pittsburgh Post-Gazette.

http://www.post-gazette.com/pg/07024/756147-114.stm

People with autism have been described as being cut off from the world around them. But a series of studies done at Carnegie Mellon University and the University of Pittsburgh have now shown that in a very real way, autistic people are also cut off from themselves.

Scans done by Carnegie Mellon’s Center for Cognitive Brain Imaging show that various regions in the brains of high-functioning autistics don’t communicate with each other as well as they do in typical people’s brains.

This basic breakdown could help explain everything from why people with autism often lack common-sense reasoning to why they don’t understand emotions and have trouble recognizing faces. In a breakthrough study three years ago, researchers at Carnegie Mellon and Pitt found that more advanced autistics were good at knowing words and their definitions, but poor at understanding the meaning of complex sentences.

Using functional magnetic resonance imaging, which measures blood flow to different parts of the brain in real time, they showed that the language-processing areas of autistics’ brains were poorly synchronized compared with nonautistic subjects. Since then, the two research centers have shown the same poor connectivity in autistics’ brains when they were playing a geometric game, and when they were at rest.

A study publicized by Carnegie Mellon last fall offers an explanation for why this might be happening. After examining how water flowed through the connective white matter that makes up about half the brain, researchers discovered that those brain cells were much more poorly organized in people with autism. The white matter sends electrical signals from one part of the brain to another, said Marcel Just, director of Carnegie Mellon’s brain imaging center.

“So why are autistics’ brain poorly synchronized?” he said. “Maybe because the cables are not quite right.” Other types of brain tests have shown the same kind of connectivity problems. At the University of Washington, researcher Michael Murias used EEGs to measure the brain waves of 18 people with autism and 18 without it. The readings from 124 electrodes on each person’s scalp showed the brain waves in people with autism were much less coordinated, particularly between the frontal lobes, where rational analysis takes place, and the rest of the brain, Dr. Murias said.

The imaging done during language tests a few years ago helped explain a phenomenon that autism researchers have long known about, said Nancy Minshew, director of Pitt’s Collaborative Programs of Excellence in Autism.

“What we see in our verbal [autistic] people across a lot of areas is that they have trouble with higher-level interpretations or understandings. They can read stories and have incredible vocabularies, but they don’t understand the real meaning of stories.” They can be especially confused if the stories don’t follow certain axioms they’ve learned, Dr. Minshew said.

She knows one young autistic man, for instance, who has read Shakespeare’s “Romeo and Juliet” more than once, “but he says, ‘I still don’t understand why Romeo and Juliet got married; it’s against the rules.’” They also have trouble with metaphors and other symbolic meanings of words, she said. She recalled sitting with a 9-year-old autistic patient one day when she told him, “We’d better get busy or we’ll be in the doghouse with your mom, and he started looking around for the doghouse.” In autistics’ brain images, the centers that recognize words and remember their definitions are often brightly lit up, Dr. Just said, but the areas of the cortex that discern the meaning of whole sentences are underactive.

People with autism have the same kind of processing problems when they try to recognize people or objects, said Mark Strauss, a research psychologist at Pitt. During normal development, babies learn at a young age to identify the differences in men’s and women’s faces, and that ability improves as they get older. Autistic children can do the same thing, Dr. Strauss said, but rather than looking at the whole face, they tend to use certain details, such as the thickness of the eyebrows or the size of the nose.

Read more: http://www.post-gazette.com/pg/07024/756147-114.stm

A Link to the actual study Center for Cognitive Brain Imaging at Carnegie Mellon University

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