Tag Archives: Social Behavior

Question?: Rett Syndrome Research

Chris asks…

Does anyone know why Rett Syndrome girls start off “normal” & then regress?

Okay I’m aware of what Rett Syndrome is & how it works (for the most part anyway) but what has me confused the most is that most of these girls develope normally for about the first 6-18 minths & then start to regress/lose skills they’ve already learned (i.e. talking, walking, eye contact) . I know this is due to a mutation in the MEPc2 gene but why/how is it they can learn things & then lose them later on. I relize the gene is responsible for turning on/off certian protiens but what is making these girls funtion properly in the beginning then? another gene maybe?

admin answers:

To quote a passage from wikipedia:
“The recent studies demonstrating that neurological deficits resulting from loss of MeCP2 can be reversed upon restoration of gene function are quite exciting because they show that neurons that have suffered the consequences of loss of MeCP2 function are poised to regain functionality once MeCP2 is provided gradually and in the correct spatial distribution. This provides hope for restoring neuronal function in patients with RTT. However, the strategy in humans will require providing the critical factors that function downstream of MeCP2 because of the challenges in delivering the correct MeCP2 dosage only to neurons that lack it, given that the slightest perturbation in MeCP2 level is deleterious. Thus, therapeutic strategies necessitate the identification of the molecular mechanisms underlying individual RTT phenotypes and picking out the candidates that can be therapeutically targeted. The next phase of research needs to assess how complete the recovery is. Clearly, lethality, level of activity, and hippocampal plasticity are rescued, but are the animals free of any other RTT symptoms such as social behavior deficits, anxiety, and cognitive impairments? Since postnatal rescue results in viability, it will be important to evaluate if even the subtler phenotypes of RTT and MECP2 disorders are rescued when protein function is restored postnatally. This is particularly important given emerging data about early neonatal experiences and their long-term effects on behavior in adults.”

What I get from that is that the nerves become damaged by the defective gene, resulting in a loss of abilities that have already been learned.

Sorry if you’ve already read this, but this is just about all I could find as far as the reason for the decline period.
Hope this helps!

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Brain Regions Critical For Social Behavior And Cognition Affected By Gene Defect, Leading To Autism-Like Behavior

Main Category: Autism
Also Included In: Genetics
Article Date: 13 Aug 2012 – 1:00 PDT Current ratings for:
Brain Regions Critical For Social Behavior And Cognition Affected By Gene Defect, Leading To Autism-Like Behavior
3 stars3 and a half stars
Scientists affiliated with the UC Davis MIND Institute have discovered how a defective gene causes brain changes that lead to the atypical social behavior characteristic of autism. The research offers a potential target for drugs to treat the condition.

Earlier research already has shown that the gene is defective in children with autism, but its effect on neurons in the brain was not known. The new studies in mice show that abnormal action of just this one gene disrupted energy use in neurons. The harmful changes were coupled with antisocial and prolonged repetitive behavior — traits found in autism.

The research is published online in the scientific journal PLoS ONE.

“A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism – how one gene defect may trigger this type of neurological behavior,” said study senior author Cecilia Giulivi, professor of molecular biosciences in the UC Davis School of Veterinary Medicine and a researcher affiliated with the UC Davis MIND Institute.

“Once you understand the mechanism, that opens the way for developing drugs to treat the condition,” she said.

The defective gene appears to disrupt neurons’ use of energy, Giulivi said, the critical process that relies on the cell’s molecular energy factories called mitochondria.

In the research, a gene called pten was tweaked in the mice so that neurons lacked the normal amount of pten’s protein. The scientists detected malfunctioning mitochondria in the mice as early as 4 to 6 weeks after birth.

By 20 to 29 weeks, DNA damage in the mitochondria and disruption of their function had increased dramatically. At this time the mice began to avoid contact with their litter mates and engage in repetitive grooming behavior. Mice without the single gene change exhibited neither the mitochondria malfunctions nor the behavioral problems.

The antisocial behavior was most pronounced in the mice at an age comparable in humans to the early teenage years, when schizophrenia and other behavioral disorders become most apparent, Giulivi said.

The research showed that, when defective, pten’s protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons. This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus – brain regions critical for social behavior and cognition.

Pten mutations previously have been linked to Alzheimer’s disease as well as a spectrum of autism disorders. The new research shows that when pten protein was insufficient, its interaction with p53 triggered deficiencies and defects in other proteins that also have been found in patients with learning disabilities including autism.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. The study’s lead author is Eleonora Napoli of UC Davis. Other study authors are Sarah Wong and James Angelastro of UC Davis.
The mice were developed at the UC Davis Mouse Biology Program by Sasha Wirth and Kent Lloyd.
The research was supported by the Autism Speaks Foundation, the MIND Institute, the Elsa U. Pardee Foundation and the National Institute of Environmental Health Sciences.
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Autism Defective Gene Link

Editor’s Choice
Academic Journal
Main Category: Autism
Also Included In: Genetics;  Neurology / Neuroscience
Article Date: 14 Aug 2012 – 11:00 PDT Current ratings for:
Autism Defective Gene Link
4 stars3 and a half stars
According to a study published online in PLoS ONE, researchers have identified how a defective gene causes brain changes that lead to the atypical social behavior characteristic of autism.

The study, conduced by researchers affiliated with the UC Davis MIND Institute, also offers a potential target for drugs to treat the condition.

Previous studies have already demonstrated that the gene is defective in children with autism, but were unable to determine its effects on neurons on the brain. In this study, the team found that in mice, the gene disrupted energy use in neurons. They found that these damaging effects were associated with antisocial and prolonged repetitive behavior – characteristics of autism.

Cecilia Giulivi, Professor of molecular biosciences in the UC Davis School of Veterinary Medicine and a researcher affiliated with the UC David MIND Institute, explained:

“A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism – how one gene defect may trigger this type of neurological behavior. Once you understand the mechanism, that opens the way for developing drugs to treat the condition.

The defective gene appears to disrupt neurons’ use of energy, the critical process that relies on the cell’s molecular energy factories called mitochondria.”

For the study, the researchers tweaked a gene called pten in mice so that neurons were deficient in the normal amount of pten’s protein. Four to six weeks after birth, the team discovered malfunctioning mitochondria in the mice.

By weeks 20-29, the team found that DNA damage in the mitochondria and disruption of their function had increased significantly. Around this time, the mice began engaging in repetitive grooming behavior and avoided contact with the other mice.

Giulivi explained: “The antisocial behavior was most pronounced in the mice at an age comparable in humans to the early teenage years, when schizophrenia and other behavioral disorders become most apparent.”

According to the researchers, when pten proteins are defective, they interact with the protein of a second gene (p53) to reduce how much energy is produced in neurons. This causes an increase in harmful mitochondria DNA changes and abnormal levels of energy production in the cerebellum and hippocampus, areas of the brain vital for cognition and social behavior.

Mutations in pten proteins have also been associated with Alzheimer’s disease and a spectrum of autism disorders. According to the researchers, when pten protein was lacking, its interaction with p53 activated deficiencies and defects in other proteins that have been identified in individuals with learning disabilities, such as autism.

The study was funded by the Autism Speaks Foundation, the MIND Institute, the Elsa U. Pardee Foundation and the National Institute of Environmental Health Sciences.

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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posted by Ken on 22 Aug 2012 at 9:23 am

Its great to find another piece of the puzzle. Placing the piece where it fits properly in the puzzle is the next step. The term “defective” being applied to genes has me curious. If something is defective that usually means that it deviates in either form or function or both. The author mentions evidence of mitochondria DNA “damage” as a result of gene pten having been “tweaked” by researchers. The DNA did not function properly which affected the neurons, because the pten had been “tweaked”. Isn’t the tweaking of the pten in effect altering form and/or function?

Damage and tweak can both be verbs (action words). Defect is either used as a noun or adverb. A “defective” gene implies a “defective” parent (sound familiar….think 1960’s). How is it that so many “defective”parents have suddenly appeared on the radar screen via their autistic offspring. Could it be that,at least in some (unknown quantity) of cases that the parents or childs genes were “damaged” or “tweaked in a way that was not previously occurrng at the rate of 1 in 108 (or whatever the lastest astronomical figure is)?

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posted by Kyle on 15 Aug 2012 at 4:38 pm

A very thought provoking article! I’m looking forward to following the research in this area. One area of possible confusion – the use of the term antisocial appears to be misused. Antisocial (as in Antisocial Personality Disorder) connotes a pattern of behavior that acts against society, such as is engaged in by sociopaths. Individuals with autism are characterized by qualitatived impairments in social interaction, better described as “asocial”. The confusion of the terms may contribute to the idea that persons affected by autistic spectrum disorders are necessarily violent or otherwise dangerous within society. They are not.

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posted by Autistic on 15 Aug 2012 at 1:42 am

Whilst you’re making undergraduate mistakes like calling genes “defective” (way to put Human Agency where it doesn’t exist), what you also fail to state is which part of the spectrum you are referring to because it has been known for a long time that unity in the Autism Spectrum genetically is a big fat lie.

Cause if it’s my end then it’s the best defective gene in the universe. Just like the tail gene in most Humans.

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‘Autism Defective Gene Link’

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Focusing On Strengths Improves Social Skills Of Adolescents With Autism

Main Category: Autism
Also Included In: Pediatrics / Children’s Health
Article Date: 04 Aug 2012 – 0:00 PDT Current ratings for:
Focusing On Strengths Improves Social Skills Of Adolescents With Autism
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The junior high and high school years are emotionally challenging even under the best of circumstances, but for adolescents with autism spectrum disorders (ASD), that time can be particularly painful. Lacking the social skills that enable them to interact successfully with their peers, these students are often ostracized and even bullied by their classmates.

However, a new study conducted by researchers at the Koegel Autism Center at UC Santa Barbara has found that by playing on their strengths – high intelligence and very specific interests – these adolescents are as capable as anyone else of forging strong friendships. In addition, the research findings demonstrate that the area of the brain that controls such social behavior is not as damaged in adolescents with ASD as was previously believed. The findings appear in a recent issue of the Journal of Positive Behavior Interventions.

“The problem is that their restricted interests can dominate their lives and further push away people they’d like to get to know,” said Robert Koegel, director of the Koegel Autism Center and the study’s lead author. He is also a professor of counseling, clinical, and school psychology and of education in UCSB’s Gevirtz Graduate School of Education. “They’re so highly focused on that interest, people think they’re weird. But by involving themselves in an activity around the interest, they not only make friends but also become valued members of the group. Their specialized skill becomes a strength.”

The research team, which also includes Lynn Koegel, the center’s clinical director, and Sunny Kim, a graduate student in education at UCSB, took a creative approach to helping three boys with ASD to interact with their peers. Rather than discourage their sometimes-obsessive interests, the researchers helped set up social clubs around them and invited students who do not have ASD to join. The clubs provided a venue for the ASD students to display their special interests and abilities, and helped them engage with their peers in a more meaningful way.

Koegel offered the example of a student with ASD who has a keen interest in computer graphics. The team created a graphic design club in which students would design logos for various companies and businesses. Because most of the students lacked the necessary expertise, they depended on their classmate with ASD to make the venture a success. “When he was able to interact on a topic in which he was interested, he was able to demonstrate more normal social behavior,” Koegel said. “He not only made friends with his fellow members, he was elected club president.”

According to Koegel, the findings are also significant because they indicate a higher degree of brain functionality than researchers had previously associated with ASD adolescents. “It has been commonly believed that the part of the brain related to social skills is so damaged that adolescents with ASD are incapable of normal social interaction,” he said. “We demonstrated that not to be the case. Once you can motivate kids to try things, they make dramatic and rapid improvement, which shows the brain is not as damaged as first thought.”

Conducted through the Koegel Center’s Eli & Edythe L. Broad Asperger Center, the study sheds important light on a period of growth and development that is presenting new issues as children who were diagnosed with ASD reach adolescence and young adulthood. “This study is so important because it suggests so much optimism,” Koegel said. “It shows the brain isn’t as damaged as people thought. And it shows that otherwise unhappy individuals can lead more fulfilling lives.”

He added that the research team was pleasantly surprised to see that the students with ASD became highly valued members of their groups, and were given a great deal of dignity and respect. They also noted that, without any instructions or encouragement from any of the researchers, many school peers enthusiastically joined in these club activities and had a great deal of enjoyment throughout and beyond the time frame of the study. “In short, this was a lot of fun for everyone,” Koegel said.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Other researchers involved with the study include John Danial, a doctoral student at UCLA; and Rosy Fredeen and Derek Rubenstein, doctoral students at UCSB at the time the research was conducted.
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‘Focusing On Strengths Improves Social Skills Of Adolescents With Autism’

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Autism: 5 Things You’ve Wondered But Never Asked

While most people understand that autism affects the brain, impairing communication and interaction skills, very few realize that scientists don’t even really know what causes it. Recent studies indicated that as many as 1 in 166 people are affected by some form of autism. With the rate so high, educating ourselves about autism is crucial. Here are a few things about autism that might surprise you.

1. Is there more than one kind of autism?

Autism Spectrum Disorder is the title that describes a group of conditions. Classic autism, which is also known as Kanner’s syndrome, is one of these. Also Asperger’s syndrome and pervasive developmental disorder (PDD). Each of these differ in expression of symptoms and even different people diagnosed with the same condition can vary in their level of functioning. Despite these different categories, autism causes developmental difficulties in three major areas: communication, social behavior, and repetitive behavior patterns.

2. What causes autism?

While there is no exact answer for what causes autism, there are several things that scientists do know. People with autism differ neurologically from those without autism. Some people may have a genetic disposition toward autism. The brain chemical, Serotonin is elevated in people with autism. While these conclusions do not seem very close to a cause, they are encouraging to families who deal with this condition. From the point of view of those whose loved ones are autistic, they want to first, find the cause, and then find the cure.

3. Is there any prevention?

Early intervention has been shown to help those with autism. While many parents don’t discover their child has autism until they are toddlers, those who identify the problem early on and seek professional assistance have a greater chance of having higher functioning children. From a report of one family with two boys with autism, the children developed normally until nearly 3 years old, when they began to slip backward cognitively and socially. It is very important to diagnose autism early, as this seems to be the only way to affect the outcome of the brain, as it is in it’s most crucial stage of development.

4. Who is more likely to be autistic?

Boys are more four times more likely to have autism than girls. This is the only discrimination that autism affords. Otherwise, autism doesn’t care about race, wealth or status, it affects all populations equally.

5. What is the treatment autism?

Autism can be treated through a combination of drugs and therapies. It is not uncommon for a child with autism to have several therapists in their home during the week. While these are not cures, they can help families manage through difficult times in an autistic child’s development. Life expectancy is no different for a person with autism than it is for the general population, so parents must think ahead to who will care for their autistic children when and if they no longer can.

Autism is a very complicated condition that affects millions of Americans. And because people with autism don’t generally display any physical signs it is hard for strangers to identify their disorder. Often, a child with autism appears out of control in a public setting, kicking, thrashing, screaming, and causing alarm to on-lookers. It is important that we all know a little more about autism so we can be more sympathetic in these situations.

Jessica Deets is passionate about autism and other disorders and volunteers her time to help organizations dedicated to overcoming physical disorders. The website at [http://www.bestautismnews.com] has more information and news about autism.

Article Source: http://EzineArticles.com/?expert=Jessica_Deets
http://EzineArticles.com/?Autism:-5-Things-Youve-Wondered-But-Never-Asked&id=87382

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Hormonal Response Is Stronger In People With Williams Syndrome, Shedding Light On The Biological Underpinnings Of Social Disorders

Main Category: Endocrinology
Also Included In: Anxiety / Stress;  Autism
Article Date: 25 Jun 2012 – 1:00 PDT Current ratings for:
‘Hormonal Response Is Stronger In People With Williams Syndrome, Shedding Light On The Biological Underpinnings Of Social Disorders’
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The hormone oxytocin – often referred to as the “trust” hormone or “love hormone” for its role in stimulating emotional responses – plays an important role in Williams syndrome (WS), according to a study published in PLoS One.

The study, a collaboration between scientists at the Salk Institute for Biological Studies and the University of Utah, found that people with WS flushed with the hormones oxytocin and arginine vasopressin (AVP) when exposed to emotional triggers.

The findings may help in understanding human emotional and behavioral systems and lead to new treatments for devastating illnesses such as WS, post-traumatic stress disorder, anxiety and possibly even autism.

“Williams syndrome results from a very clear genetic deletion, allowing us to explore the genetic and neuronal basis of social behavior,” says Ursula Bellugi, the director of Salk’s Laboratory for Cognitive Neuroscience and a co-author on the paper. “This study provides us with crucial information about genes and brain regions involved in the control of oxytocin and vasopressin, hormones that may play important roles in other disorders.”

WS arises from a faulty recombination event during the development of sperm or egg cells. As a result, virtually everyone with WS has exactly the same set of genes missing (25 to 28 genes are missing from one of two copies of chromosome 7). There also are rare cases of individuals who retain one or more genes that most people with the disorder have lost.

To children with WS, people are much more comprehensible than inanimate objects. Despite myriad health problems they are extremely gregarious, irresistibly drawn to strangers, and insist on making eye contact. They have an affinity for music. But they also experience heightened anxiety, have an average IQ of 60, experience severe spatial-visual problems, and suffer from cardiovascular and other health issues. Despite their desire to befriend people, they have difficulty creating and maintaining social relationships, something that is not at all understood but can afflict many people without WS.

In the new study, led by Dr. Julie R. Korenberg, a University of Utah professor and Salk adjunct professor, the scientists conducted a trial with 21 participants, 13 who have WS and a control group of eight people without the disorder. The participants were evaluated at the Cedars-Sinai Medical Center in Los Angeles. Because music is a known strong emotional stimulus, the researchers asked participants to listen to music.

Before the music was played, the participants’ blood was drawn to determine a baseline level for oxytocin, and those with WS had three times as much of the hormone as those without the syndrome. Blood also was drawn at regular intervals while the music played and was analyzed afterward to check for real-time, rapid changes in the levels of oxytocin and AVP. Other studies have examined how oxytocin affects emotion when artificially introduced into people, such as through nasal sprays, but this is one of the first significant studies to measure naturally occurring changes in oxytocin levels in rapid, real time as people undergo an emotional response.

There was little outward response to the music, but when the blood samples were analyzed, the researchers were happily surprised. The analyses showed that the oxytocin levels, and to a lesser degree AVP, had not only increased but begun to bounce among WS participants while among those without WS, both the oxytocin and AVP levels remained largely unchanged as they listened to music.

Korenberg believes the blood analyses strongly indicate that oxytocin and AVP are not regulated correctly in people with WS, and that the behavioral characteristics unique to people with WS are related to this problem.

“This shows that oxytocin quite likely is very involved in emotional response,” Korenberg says.

To ensure accuracy of results, those taking the test also were asked to place their hands in 60-degree Fahrenheit water to test for negative stress, and the same results were produced as when they listened to music. Those with WS experienced an increase in oxytocin and AVP, while those without the syndrome did not.

In addition to listening to music, study participants already had taken three social behavior tests that evaluate willingness to approach and speak to strangers, emotional states, and various areas of adaptive and problem behavior. Those test results suggest that increased levels of oxytocin are linked to both increased desire to seek social interaction and decreased ability to process social cues, a double-edged message that may be very useful at times, for example, during courtship, but damaging at others, as in WS.

“The association between abnormal levels of oxytocin and AVP and altered social behaviors found in people with Williams Syndrome points to surprising, entirely unsuspected deleted genes involved in regulation of these hormones and human sociability,” Korenberg said. “It also suggests that the simple characterization of oxytocin as ‘the love hormone’ may be an overreach. The data paint a far more complicated picture.”

In particular, the study results indicate that the missing genes affect the release of oxytocin and AVP through the hypothalamus and the pituitary gland. About the size of a pearl, the hypothalamus is located just above the brain stem and produces hormones that control body temperature, hunger, mood, sex drive, sleep, hunger and thirst, and the release of hormones from many glands, including the pituitary. The pituitary gland, about the size of a pea, controls many other glands responsible for hormone secretion.

Overall, the researchers say, their findings paint a very hopeful picture, and the study holds promise for speeding progress in treating WS, and perhaps Autism and anxiety through regulation of these key players in human brain and emotion, oxytocin and vasopressin.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our endocrinology section for the latest news on this subject. The study was funded by the National Institutes of Health and the McDonnell Foundation.
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Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits

Main Category: Autism
Article Date: 21 May 2012 – 0:00 PDT Current ratings for:
‘Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits’
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Preliminary results from an ongoing, large-scale study by Yale School of Medicine researchers shows that oxytocin – a naturally occurring substance produced in the brain and throughout the body – increased brain function in regions that are known to process social information in children and adolescents with autism spectrum disorders (ASD).

A Yale Child Study Center research team that includes postdoctoral fellow Ilanit Gordon and Kevin Pelphrey, the Harris Associate Professor of Child Psychiatry and Psychology, presented the results at the International Meeting for Autism Research.

“Our findings provide the first, critical steps toward devising more effective treatments for the core social deficits in autism, which may involve a combination of clinical interventions with an administration of oxytocin,” said Gordon. “Such a treatment approach will fundamentally improve our understanding of autism and its treatment.”

Social-communicative dysfunctions are a core characteristic of autism, a neurodevelopmental disorder that can have an enormous emotional and financial burden on the affected individual, their families, and society.

Gordon said that while a great deal of progress has been made in the field of autism research, there remain few effective treatments and none that directly target the core social dysfunction. Oxytocin has recently received attention for its involvement in regulating social abilities because of its role in many aspects of social behavior and social cognition in humans and other species.

To assess the impact of oxytocin on the brain function, Gordon and her team conducted a first-of-its-kind, double-blind, placebo-controlled study on children and adolescents aged 7 to 18 with ASD. The team members gave the children a single dose of oxytocin in a nasal spray and used functional magnetic resonance brain imaging to observe its effect.

The team found that oxytocin increased activations in brain regions known to process social information. Gordon said these brain activations were linked to tasks involving multiple social information processing routes, such as seeing, hearing, and processing information relevant to understanding other people.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Other authors on the study include Randi H. Bennett, Brent C. vander Wyk, James F. Leckman, and Ruth Feldman.
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‘Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits’

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Clues To Autism Mystery Offered By Novel Mouse Model

Main Category: Autism
Article Date: 22 Mar 2012 – 0:00 PDT

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Early disruptions in serotonin signaling in the brain may contribute to autism spectrum disorder (ASD), and other “enduring effects on behavior,” Vanderbilt University researchers report.

Serotonin is a brain chemical that carries signals across the synapse, or gap between nerve cells. The supply of serotonin is regulated by the serotonin transporter (SERT). In 2005, a team of Vanderbilt researchers led by Randy Blakely and James Sutcliffe identified rare genetic variations in children with ASD that disrupt SERT function.

In a new study published this week in the Proceedings of the National Academy of Sciences (PNAS), the researchers report the creation of a mouse model that expressed the most common of these variations.

The change is a very small one in biochemical terms, yet it appears to cause SERT in the brain to go into “overdrive” and restrict the availability of serotonin at synapses.

“The SERT protein in the brain of our mice appears to exhibit the exaggerated function and lack of regulation we saw using cell models,” said Blakely, director of the Vanderbilt Silvio O. Conte Center for Neuroscience Research.

“Remarkably, these mice show changes in social behavior and communication from early life that may parallel aspects of ASD,” noted first author Jeremy Veenstra-VanderWeele, assistant professor of Psychiatry, Pediatrics and Pharmacology.

The researchers conclude that a lack of serotonin during development may lead to long-standing changes in the way the brain is “wired.”

In 1961, investigators at Yale discovered that as many as 30 percent of children with autism have elevated blood levels of serotonin, a finding described as “hyperserotonemia.”

Since then, these findings have been replicated many times. Indeed, hyperserotonemia is the most consistently reported biochemical finding in autism, and is a highly inherited trait. Yet, the cause or significance of this “bio-marker” has remained shrouded in mystery.

Until now. In the current study, Veenstra-VanderWeele, Blakely and their colleagues showed that they could produce hyperserotonemia in mice that express a variant of a human SERT gene associated with autism.

Because the genetic change makes the transporter more active, higher levels of serotonin accumulate in platelets and therefore in the bloodstream. In the brain, overactive transporters should have the opposite effect – lowering serotonin levels at the synapse and producing behavioral changes relevant to autism. That’s exactly what the researchers observed.

Of course, no mouse model can completely explain or reproduce the human condition. Neither does a single genetic variation cause autism. Experts believe the wide spectrum of autistic behaviors represents a complex web of interactions between many genes and environmental factors.

But animal models are critical to exploring more deeply the basis for the developmental changes that are observed in ASD. The scientists are using these mice to explore how altered brain serotonin levels during development may produce long-lasting changes in behavior and impact the risk for autism.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Scientists from the National Institute of Mental Health, the Medical University of South Carolina and the University of Texas Health Science Center in San Antonio contributed to the study.
The research was supported by the National Institutes of Health, the advocacy organization Autism Speaks and the American Academy of Child and Adolescent Psychiatry.
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Autism: 5 Things You’ve Wondered But Never Asked

While most people understand that autism affects the brain, impairing communication and interaction skills, very few realize that scientists don’t even really know what causes it. Recent studies indicated that as many as 1 in 166 people are affected by some form of autism. With the rate so high, educating ourselves about autism is crucial. Here are a few things about autism that might surprise you.

1. Is there more than one kind of autism?

Autism Spectrum Disorder is the title that describes a group of conditions. Classic autism, which is also known as Kanner’s syndrome, is one of these. Also Asperger’s syndrome and pervasive developmental disorder (PDD). Each of these differ in expression of symptoms and even different people diagnosed with the same condition can vary in their level of functioning. Despite these different categories, autism causes developmental difficulties in three major areas: communication, social behavior, and repetitive behavior patterns.

2. What causes autism?

While there is no exact answer for what causes autism, there are several things that scientists do know. People with autism differ neurologically from those without autism. Some people may have a genetic disposition toward autism. The brain chemical, Serotonin is elevated in people with autism. While these conclusions do not seem very close to a cause, they are encouraging to families who deal with this condition. From the point of view of those whose loved ones are autistic, they want to first, find the cause, and then find the cure.

3. Is there any prevention?

Early intervention has been shown to help those with autism. While many parents don’t discover their child has autism until they are toddlers, those who identify the problem early on and seek professional assistance have a greater chance of having higher functioning children. From a report of one family with two boys with autism, the children developed normally until nearly 3 years old, when they began to slip backward cognitively and socially. It is very important to diagnose autism early, as this seems to be the only way to affect the outcome of the brain, as it is in it’s most crucial stage of development.

4. Who is more likely to be autistic?

Boys are more four times more likely to have autism than girls. This is the only discrimination that autism affords. Otherwise, autism doesn’t care about race, wealth or status, it affects all populations equally.

5. What is the treatment autism?

Autism can be treated through a combination of drugs and therapies. It is not uncommon for a child with autism to have several therapists in their home during the week. While these are not cures, they can help families manage through difficult times in an autistic child’s development. Life expectancy is no different for a person with autism than it is for the general population, so parents must think ahead to who will care for their autistic children when and if they no longer can.

Autism is a very complicated condition that affects millions of Americans. And because people with autism don’t generally display any physical signs it is hard for strangers to identify their disorder. Often, a child with autism appears out of control in a public setting, kicking, thrashing, screaming, and causing alarm to on-lookers. It is important that we all know a little more about autism so we can be more sympathetic in these situations.

Jessica Deets is passionate about autism and other disorders and volunteers her time to help organizations dedicated to overcoming physical disorders. The website at [http://www.bestautismnews.com] has more information and news about autism.

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Tagged as: Autism, autism faq, autism questions

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How a Hug Can Help Your Autistic Child

Autistic children and adults often seek pressure in a variety of ways to calm themselves and cope with sensory overload. Oftentimes, hugs and squeezes from other people can cause more distress because autistic children or adults are often unable to communicate their needs by indicating a particular amount or length of pressure. This is both frustrating and ineffective for both the autistic person and whoever is hugging or squeezing them.

The hug machine was created to help relive this frustration, putting autistic individuals in control of their situation. Both children and adults who suffer from autism sometimes crave pressure to help calm anxiety. Because of this, one woman with autism developed the hug machine, also known as a hug box or a squeeze machine. The hug machine has two padded sideboards connected near the bottom of the boards to form a V-shape. A lever helps push the sideboards together to create pressure; the lever also allows the autistic child or adult the ability to control the amount and length of pressure.

Studies are still being conducted to find out why those with autism respond to pressure and how it can produce a calming effect. The hug machine may affect the heightened sensory perceptions of those with autism who often feels disruptive or distressing behavior. By applying pressure, perhaps the autistic child or adult moves his or her focus to a single feeling-the pressure-which in turn produces a calming effect. For many autistic children and adults, anxiety can be completely incapacitating. Not being able to function with the anxiety is frustrating, and so appropriate social behavior is even more difficult. Sometimes, the only release from such anxiety is through pressure. To this day, the hug machine is used by several programs and researchers studying autism as well as therapy programs.

Remember that hugging or squeezing an autistic child may not help him or her. You may, in fact, increase their senses and cause more anxiety. Though you may not be able to purchase a hug machine, you may be able to create a similar object. Try wrapping the autistic child or adult in a blanket, where they can control how much pressure to apply. You can also look into buying padded boards that more closely simulate the hug machine’s side-boards and perhaps tie or tape some heavy-duty yarn to each side to allow the autistic child or adult control over how much pressure to apply and for how long. Contact your child’s school to see if there has been any interest in purchasing a community hug-machine. This may not be a cure to all your child’s problems, but it works well to help many autistic individuals cope with the world.

To learn about early signs of autism and mild autism, visit Autism Diagnosis.
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