The Autistic Neuron: Troubled Translation?

被引：453

作者：

Kelleher, Raymond J., III ^{[1
,2
,3
]}

Bear, Mark F. ^{[4
,5
]}

机构：

[1] Harvard Univ, Sch Med, Harvard Partners Ctr, Ctr Human Genet Res, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Program Neurosci,Autism Consortium, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA

[4] Howard Hughes Med Inst, Picower Inst Learning & Memory, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA

[5] MIT, Autism Consortium, Boston, MA 02115 USA

来源：

CELL | 2008年 / 135卷 / 03期

关键词：

D O I：

10.1016/j.cell.2008.10.017

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Autism is a complex genetic disorder, but single-gene disorders with a high prevalence of autism offer insight into its pathogenesis. Recent evidence suggests that some molecular defects in autism may interfere with the mechanisms of synaptic protein synthesis. We propose that aberrant synaptic protein synthesis may represent one possible pathway leading to autistic phenotypes, including cognitive impairment and savant abilities.

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收藏

页码：401 / 406

页数：6

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