期刊
MOLECULAR PSYCHIATRY
卷 17, 期 7, 页码 682-693出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2011.139
关键词
genetic; mental retardation; signaling pathways; synapse
资金
- ANR [ANR-08-MNPS-037-04, ANR 2010-Neuro-001-01, ANR-2010-BLAN-1434-03]
- European Union [241995]
- Fondation Jerome Lejeune
- INSERM
- 'Ministere de l'Education Nationale'
- SUNY
Genetic causes of intellectual disability (ID) include mutations in proteins with various functions. However, many of these proteins are enriched in synapses and recent investigations point out their crucial role in the subtle regulation of synaptic activity and dendritic spine morphogenesis. Moreover, in addition to genetic data, functional and animal model studies are providing compelling evidence that supports the emerging unifying synapse-based theory for cognitive deficit. In this review, we highlight ID-related gene products involved in synaptic morphogenesis and function, with a particular focus on the emergent signaling pathways involved in synaptic plasticity whose disruption results in cognitive deficit. Molecular Psychiatry (2012) 17, 682-693; doi:10.1038/mp.2011.139; published online 25 October 2011
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