 | Health/Science Healthcare and fitness updates. Science news on biology, space, the environment, health, NASA, weather, drugs, heart disease, cancer, AIDS, mental health, etc. | | Welcome to the Foire d'Opinions Haitiennes forums. You are currently viewing our boards as a guest which gives you limited access to view most discussions and access our other features. By joining our free community you will have access to post topics, communicate privately with other members (PM), respond to polls, upload content and access many other special features. Registration is fast, simple and absolutely free so please, join our community today! If you have any problems with the registration process or your account login, please contact contact us. | Autistic kids have some brain abnormalities
|  Featured Articles | | | Article Tools | | | | | | |  Autistic kids have some brain abnormalities
Autistic kids have brain abnormalities
Those with disability have more gray matter in some areas, study says
Reuters
updated 2:00 p.m. ET, Wed., Nov. 28, 2007
CHICAGO - Autistic children have more gray matter in areas of the brain that control social processing and sight-based learning than children without the developmental disability, a small study said on Wednesday.
Researchers combined two sophisticated imaging techniques to track the motion of water molecules in the brain and pinpoint small changes in gray matter volume in 13 boys with high-functioning autism or Asperger syndrome and 12 healthy adolescents. Their average age was 11.
The autistic children were found to have enlarged gray matter in the parietal lobes of the brain linked to the mirror neuron system of cells associated with empathy, emotional experience and learning through sight.
Those children also showed a decrease in gray matter volume in the right amygdala region of the brain that correlated with degrees of impairment in social interaction, the study found.
The researchers assessed patient brain function using a combination of diffusion tensor imaging (DTI) and a new imaging method called apparent diffusion coefficient based morphometry (ABM). Their findings were presented at the annual meeting of the Radiological Society of North America in Chicago.
Unlike earlier technology, the technique can detect subtle changes in thousands of small sections of the brain, said the study's lead author, Manzar Ashtari of the Children's Hospital of Philadelphia. "Now we have sharper tools," Ashtari said in an interview.
Larger amounts of gray matter in the left parietal area of the brain correlated with higher IQs in the control group of children but not in the autistic children, because that section of gray matter is not functioning properly, Ashtari said.
Autism affects about 1.5 million Americans, according to the Centers for Disease Control and Prevention. Considered the fastest-growing developmental disability in the United States, autism typically appears in the first three years of life and hinders social interaction and communication skills.
More studies that look at brain structure and function together are needed to better understand how the minds of autistic children work, Ashtari said, with the hope of devising earlier intervention strategies to treat the condition.
"If more and more people truly prove that mirror neurons in general are responsible and are involved in children with autism, then I believe more and more people will think, how do we actually strengthen them? What can we do to make them actually work normally?" Ashtari said. | | | | | | Fever can unlock autism's grip
Fever can unlock autism's grip
Elevated temperature can restore cell communication in brain, study finds
Reuters
updated 9:54 a.m. ET, Mon., Dec. 3, 2007
CHICAGO - Fever can temporarily unlock autism's grip on children, a finding that could shed light on the roots of the condition and perhaps provide clues for treatment, researchers reported on Monday.
It appears that fever restores nerve cell communications in regions of the autistic brain, restoring a child's ability to interact and socialize during the fever, the study said.
"The results of this study are important because they show us that the autistic brain is plastic, or capable of altering current connections and forming new ones in response to different experiences or conditions," said Dr. Andrew Zimmerman, a pediatric neurologist at Baltimore's Kennedy Krieger Institute, who was one of the study authors.
The study, published in the journal Pediatrics, was based on 30 children with autism aged 2 to 18 who were observed during and after a fever of at least 100.4 degrees Fahrenheit.
More than 80 percent of those with fever showed some improvements in behavior during it and 30 percent had dramatic improvements, the researchers said. The change involved things like longer concentration spans, more talking, improved eye contact and better overall relations with adults and other children.
Zimmerman's team said the fever effect had been noted anecdotally in the past by parents and doctors.
Lee Grossman, president and chief executive officer of the Autism Society of America, said he had noticed it in his own son, who is now 20.
But he noted in an interview that the study's authors said expanded research was needed on the fever effect and its implications. "It's good that they've noticed this and are bringing it forward," he said.
Reconnecting autistic brain
People with autism spectrum disorders suffer in varying degrees from limited social interactions, lack of verbal and non-verbal communication and other abilities.
As many as 1.5 million Americans have some form of autism, according to ASA. It is not known what causes the condition.
Zimmerman said that while there currently is no definitive medical treatment, speech and language therapy started as soon as possible after diagnosis "can make a significant difference."
He called the fever research, headed by colleague Laura Curran, "an exciting lead" that could help point the way to a treatment that would reconnect the autistic brain. He said the fever effect was believed found only in children, whose brains are more "plastic" than those of adults. | | | | | Gene tinkering curbs autism in mice
Gene tinkering curbs autism in mice
Pill in the pipeline could have same effect in people, scientists say
updated 2:29 p.m. ET, Wed., Dec. 19, 2007
Scientists could be on the verge of a new treatment for autism, if the results of animal research hold up in people. A study in mice suggests that several drugs, including one that is poised to enter trials in human patients as soon as next year, could improve brain function and reverse the symptoms of some autistic patients.
So far, the research indicates the drugs will only be effective for one form of autism that is caused by a mutation of a gene on the X chromosome, a condition known as fragile X syndrome. But the researchers think there's a possibility the medications could also work for other cases of autism where the cause is unknown.
“I really hope that we can go beyond fragile X and see significant improvement in children with other types of autism,” said Mark Bear, a neuroscientist at the Massachusetts Institute of Technology who led the mice research.
Autism disorders strike 1 out of every 150 children. Currently there is no cure for autism, a complex developmental disorder that impairs a person’s ability to communicate and relate with others and is associated with a range of unusual repetitive behaviors, such as obsessively arranging objects.
The exact cause of the disorder remains elusive but it has been linked to a variety of genes, including the fragile X mutation that can lead to both mental retardation and autism. Most patients with fragile X will show some autism symptoms and about 20 percent will meet the criteria to be considered autistic. The mutation is thought to lead to mental problems because it causes hyperactivity of a brain protein called metabotropic glutamate receptor 5 (mGluR5) that normally plays a role in learning and memory.
A team led by Bear wondered if reducing levels of mGluR5 protein could restore normal brain function. The researchers used a combination of genetic engineering and selective breeding to produce a line of mice that had both the fragile X mutation and toned down levels of the mGluR5 protein in their brain. The intent was to get an idea of what would happen when the protein was suppressed using a drug in human patients.
In a finding that the researchers described as “remarkable” in Thursday’s issue of the scientific journal Neuron, the mice — which should have had mental retardation and autism-like symptoms due to the fragile X mutation — instead showed near-normal brain function and memory.
Pill in the works
That was exciting in and of itself, because it indicated that blocking the mGluR5 protein could lead to improvements in some forms of autism and mental retardation. But Bear said the even more provocative implication is that a compound that does just that already exists. A few years ago, he founded Seaside Therapeutics, a small pharmaceutical firm in Cambridge, Mass., that is developing a mGluR5-blocking drug called STX107. The agent, which would be taken as a pill, has passed all the safety studies required for beginning studies in people.
Randall Carpenter, Seaside's president and chief executive officer, said he's “cautiously optimistic,” about STX107's potential to reverse autism symptoms in people. “These are really exciting findings, but we really don't know how helpful it's going to be until we test it in humans,” he said.
Seaside now plans to meet with the Food and Drug Administration to request approval to begin clinical trials involving people with fragile X syndrome and autism. Carpenter anticipates starting the initial human studies sometime next year.
Outside researchers also were enthusiastic about the potential of the compound.
“It seems very promising indeed,” said Matthew Belmonte, a neuroscientist at Cornell University's Department of Human Development. He said the study in mice suggests that drugs that suppress mGluR5 can restore brain function without causing any other ill effects. That bodes well for human trials, Belmonte said, but he noted that suppressing a gene in an animal study is not the same as using a drug in people so there could be unforeseen risks that may turn up.
Not everyone is on board, however. Sophia Colamarino, a neurobiologist and vice president of research for the advocacy group Autism Speaks, which helped fund Bear's research, said the finding “give us hope” that this could be a viable strategy for treating autism, but she added that it's too early to tell whether STX107 will improve autistic behaviors in people. The drug could reduce mGluR5 levels, but autism is such a complex disease, this may not be enough to restore normal behavior in patients, Colamarino said.
Two other drugs in the works
If the drug does fail, there still may be hope for patients and their families. The Fragile X Research Foundation (FRAXA), which co-funded STX107 research, is supporting investigations involving two other drugs that block the same protein.
Lithium, which is used for treating depression and bipolar disorder, is being investigated for its potential to treat autism and fragile X by researchers at Rush University in Chicago.
And another compound called fenobam — initially developed as an anti-anxiety medication in the 1970s and then abandoned — is being revitalized for fragile X by Neuropharm, a Surrey, UK-based pharmaceutical company.
“We believe that drugs which block mGluR5 have enormous potential for the treatment of fragile X and related developmental disorders, including many cases of autism,” said Katie Clapp, president and executive director of FRAXA. | | | | | Rare genetic glitch hikes risk of autism
Rare genetic glitch hikes risk of autism
Finding instills hope for better understanding, treatment of disorder
The Associated Press
updated 5:18 p.m. ET, Wed., Jan. 9, 2008
A rare genetic variation dramatically raises the risk of developing autism, a large study showed, opening new research targets for better understanding the disorder and for treating it.
Research into the causes of autism has focused on genetic causes because so many families have multiple children with the disorder. Thus far, only about 10 percent of autism cases have a known genetic cause. Boston-area researchers estimate the gene glitch they’ve identified accounts for another 1 percent of cases.
They found a segment of a chromosome which has genes linked to brain development and various developmental disorders was either missing or duplicated far more often in autistic people. The defect was inherited in some cases, but more often the result of a random genetic accident.
The results from the Autism Consortium study, released online Wednesday by the New England Journal of Medicine, confirm those of smaller studies by U.S. and Canadian research groups in the past year. The consortium verified its findings by checking two other DNA databases.
“They really did nail it,” said Dr. Andrew Zimmerman, director of the Kennedy Krieger Institute’s Center for Autism & Related Disorders in Baltimore, who was not involved in the research.
He predicted children newly diagnosed with autism or other developmental disorders now will be tested for this defect on chromosome 16 and that studies of many more DNA samples may reveal other autism-related gene variations.
Already, the findings are starting to be used to give some parents long-sought answers to burning questions: What caused autism in their child and how likely is it that any future children also would have autism, long known to run in families?
“We’ve provided very compelling evidence that this particular small stretch of the genome provides an important clue to the biological roots of autism,” said lead researcher Mark J. Daly, an assistant genetics professor at Harvard Medical School and an investigator for the consortium, which includes researchers from 14 Boston-area universities and medical centers.
When the biological pathways involved are figured out, scientists can try to design drugs to target chemicals in the brain to treat autism, said Geraldine Dawson, chief science officer of the advocacy group Autism Speaks.
“I think chromosome 16 is now going to be a hotbed for autism research,” said Thomas Lehner, head of the genomic research branch at the National Institute of Mental Health. “It gives us a very important lead.”
Another study researcher, Dr. David Miller of Children’s Hospital Boston, said the chromosome 16 variations increased the risk of autism a hundredfold. But he said the disorder must be due to a combination of genetic variations since there were cases of people who had the defect but didn’t have autism.
Autism, a complex, poorly understood disorder, is characterized by repetitive behaviors and poor social interaction and communication skills. Research has mainly centered on genetic causes, and on whether it could be caused by the mercury-based preservative once used in childhood vaccines, which has been repeatedly discounted.
The number of children diagnosed with autism has risen in recent years to as many as one in 150 American children, but experts are unsure whether its prevalence really is increasing or the trend is due to a broader definition of autism.
For their study, consortium researchers scanned all 46 chromosomes from DNA samples from 1,441 children with autism or related disorders. They also scanned DNA from most of their parents and 2,800 other people, none known to have autism.
The researchers found a 25-gene segment of chromosome 16 was missing in five children with autism; none of their parents had the deletion. That shows that in some cases the genetic glitch is not inherited from the parents, but instead due to a random accident while an egg or sperm is being formed.
Another seven autistic children had a chromosome 16 duplication, but all but one had parents with the same duplication.
The researchers confirmed their findings by looking at DNA databases from Children’s Hospital Boston and Iceland. The same defect was found in 1 percent of those with autism or related disorders. It was found in just seven of about 19,000 Iceland samples from people without the disorder. | | | | Article Tools | Search this Article | | | | | Display Modes |  Linear Mode |  Posting Rules | You may not post new articles You may not post comments You may not post attachments You may not edit your posts
HTML code is Off
Points Per Thread View: 2.00 Points Per Thread: 15.00 Points Per Reply: 10.00 | | | |
