期刊
ANNUAL REVIEW OF NEUROSCIENCE, VOL 33
卷 33, 期 -, 页码 221-243出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-neuro-060909-153215
关键词
Ras; GABA; LTP; animal model; neurodevelopmental disorder; ADHD
资金
- NATIONAL INSTITUTE OF MENTAL HEALTH [T32MH019384] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038480] Funding Source: NIH RePORTER
- NIMH NIH HHS [T32 MH019384, 2T32MH019384-11A2] Funding Source: Medline
- NINDS NIH HHS [R01 NS038480-08, R01 NS038480, R01 NS38480] Funding Source: Medline
Neurofibromatosis Type I (NF1) is a single-gene disorder characterized by a high incidence of complex cognitive symptoms, including learning disabilities, attention deficit disorder, executive function deficits, and motor coordination problems. Because the underlying genetic cause of this disorder is known, study of NF1 from a molecular, cellular, and systems perspective has provided mechanistic insights into the etiology of higher-order cognitive symptoms associated with the disease. In particular, studies of animal models of NF1 indicated that disruption of Ras regulation of inhibitory networks is critical to the etiology of cognitive deficits associated with NF1. Animal models of Nf1 identified mechanisms and pathways that are required for cognition, and represent an important complement to the complex neuropsychological literature on learning disabilities associated with this condition. Here, we review findings from NF1 animal models and human populations affected by NF1, highlighting areas of potential translation and discussing the implications and limitations of generalizing findings from this single-gene disease to idiopathic learning disabilities.
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