Drugs Hint At Potential Reversal Of Autism
richie
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Drugs Hint At Potential Reversal Of Autism
Morning Edition, September 23, 2008 · Scientific researchers can spend years in the lab on obscure topics, like how a sea slug remembers or how a fruit fly sees color. But every now and then, a basic scientist makes a discovery that changes human lives.
Mark Bear, who directs the Picower Institute for Learning and Memory at MIT, is one of those basic scientists. He's discovered a system in the brain that could change the lives of thousands of people with the genetic disorder known as Fragile X Syndrome.....
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Oh, damn. I really wish these fringe scientists would cut this sort of nonsense out...
"fragile x causes mental retardation and autism". Yeah... Right.
How about "fragile x causes mental retardation and may indicate a minor factor in the development of autism, research pending."
Junior league dickheads...
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Oh, well, fancy that! Isn't that neat, eh?
They aren't the same, but people with fragile X are far, far more likely to have autism than the average person. People with fragile X also commonly have neural network hyperexcitability. So even though most with ASDs don't have fragile X, this research may be of high value to the ASD community.
One other note: some of the basic research for this came out of feeding Monosodium Glutamate to various genotypes of fruit flies to model the type of nervous dysfunction seen in fragile X and ASDs.
Identification of small molecules rescuing fragile X syndrome phenotypes in Drosophila.
Chang S, Bray SM, Li Z, Zarnescu DC, He C, Jin P, Warren ST.
Department of Human Genetics, Emory University School of Medicine, 615 Michael Street Suite 300, Atlanta, Georgia 30322, USA.
Fragile X syndrome is caused by the functional loss of the fragile X mental retardation 1 (FMR1) gene. Deletion of the FMR1 ortholog in Drosophila melanogaster (Fmr1) recapitulates many phenotypes associated with fragile X syndrome. We have discovered that Fmr1 mutant Drosophila die during development when reared on food containing increased levels of glutamate, which is consistent with the theory that FMR1 loss results in excess glutamate signaling. Using this lethal phenotype, we screened a chemical library of 2,000 compounds and identified nine molecules that rescued the lethality, including three that implicate the GABAergic inhibitory pathway. Indeed, GABA treatment rescued several known Fmr1 mutant phenotypes in flies, including mushroom bodies defects, excess Futsch translation and abnormal male courtship behavior. These data are consistent with GABAergic inhibition of the enhanced excitatory pathway in fragile X syndrome. In addition, our screen reveals that the muscarinic cholinergic receptors may have a role in fragile X syndrome in parallel to the GABAergic pathway. These results point to potential therapeutic approaches for treating fragile X syndrome.
Identification of small molecules rescuing fragile X syndrome phenotypes in Drosophila.
Chang S, Bray SM, Li Z, Zarnescu DC, He C, Jin P, Warren ST.
Department of Human Genetics, Emory University School of Medicine, 615 Michael Street Suite 300, Atlanta, Georgia 30322, USA.
Fragile X syndrome is caused by the functional loss of the fragile X mental retardation 1 (FMR1) gene. Deletion of the FMR1 ortholog in Drosophila melanogaster (Fmr1) recapitulates many phenotypes associated with fragile X syndrome. We have discovered that Fmr1 mutant Drosophila die during development when reared on food containing increased levels of glutamate, which is consistent with the theory that FMR1 loss results in excess glutamate signaling. Using this lethal phenotype, we screened a chemical library of 2,000 compounds and identified nine molecules that rescued the lethality, including three that implicate the GABAergic inhibitory pathway. Indeed, GABA treatment rescued several known Fmr1 mutant phenotypes in flies, including mushroom bodies defects, excess Futsch translation and abnormal male courtship behavior. These data are consistent with GABAergic inhibition of the enhanced excitatory pathway in fragile X syndrome. In addition, our screen reveals that the muscarinic cholinergic receptors may have a role in fragile X syndrome in parallel to the GABAergic pathway. These results point to potential therapeutic approaches for treating fragile X syndrome.
So that could explain why I feel better after eating Chinese food, lol.
Ravenclawgurl
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So what happens to the few that actually do happen to have fragile X AND autism? They cure the fragile X, and the autism is still there?
So what happens to the few that actually do happen to have fragile X AND autism? They cure the fragile X, and the autism is still there?
It won't cure fragile X, but it seems to treat it - resulting in improvements that include neurological function.
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