Document Detail


A synaptic trek to autism.
MedLine Citation:
PMID:  19545994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autism spectrum disorders (ASD) are diagnosed on the basis of three behavioral features namely deficits in social communication, absence or delay in language, and stereotypy. The susceptibility genes to ASD remain largely unknown, but two major pathways are emerging. Mutations in TSC1/TSC2, NF1, or PTEN activate the mTOR/PI3K pathway and lead to syndromic ASD with tuberous sclerosis, neurofibromatosis, or macrocephaly. Mutations in NLGN3/4, SHANK3, or NRXN1 alter synaptic function and lead to mental retardation, typical autism, or Asperger syndrome. The mTOR/PI3K pathway is associated with abnormal cellular/synaptic growth rate, whereas the NRXN-NLGN-SHANK pathway is associated with synaptogenesis and imbalance between excitatory and inhibitory currents. Taken together, these data strongly suggest that abnormal synaptic homeostasis represent a risk factor to ASD.
Authors:
Thomas Bourgeron
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2009-06-21
Journal Detail:
Title:  Current opinion in neurobiology     Volume:  19     ISSN:  1873-6882     ISO Abbreviation:  Curr. Opin. Neurobiol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-07-27     Completed Date:  2009-10-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9111376     Medline TA:  Curr Opin Neurobiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  231-4     Citation Subset:  IM    
Affiliation:
Human Genetics and Cognitive Functions, Institut Pasteur, 25 rue du Docteur Roux, 75015 Paris, France. thomasb@pasteur.fr
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MeSH Terms
Descriptor/Qualifier:
Animals
Autistic Disorder / genetics*,  physiopathology*
Brain / growth & development,  physiopathology
Humans
Neural Inhibition / genetics,  physiology
Neural Pathways / growth & development,  physiopathology
Neurons / physiology
Synapses / genetics*,  physiology*

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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