期刊
NATURE REVIEWS NEUROSCIENCE
卷 16, 期 9, 页码 551-563出版社
NATURE RESEARCH
DOI: 10.1038/nrn3992
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资金
- Institut Pasteur
- Fondation Bettencourt Schueller
- Centre National de la Recherche Scientifique
- University Paris Diderot
- Agence Nationale de la Recherche (SynDivAutism)
- Conny-Maeva Charitable Foundation
- Fondation Cognacq-Jay
- Orange Foundation
- Fondation FondaMental
- Innovative Medicines Initiative [115300]
- European Union's Seventh Framework Programme (FP7)
- European Federation of Pharmaceutical Industries and Associations (EFPIA)
Genetics studies of autism spectrum disorder (ASD) have identified several risk genes that are key regulators of synaptic plasticity. Indeed, many of the risk genes that have been linked to these disorders encode synaptic scaffolding proteins, receptors, cell adhesion molecules or proteins that are involved in chromatin remodelling, transcription, protein synthesis or degradation, or actin cytoskeleton dynamics. Changes in any of these proteins can increase or decrease synaptic strength or number and, ultimately, neuronal connectivity in the brain. In addition, when deleterious mutations occur, inefficient genetic buffering and impaired synaptic homeostasis may increase an individual's risk for ASD.
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