期刊
CLINICAL NEUROPHARMACOLOGY
卷 34, 期 6, 页码 203-205出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNF.0b013e31823a1247
关键词
CHRNA7; microdeletions; alpha 7 nicotinic acetylcholine receptors; autism spectrum disorders
Recurrent microdeletions of chromosome 15q13.3 are causally associated with autism spectrum disorders (ASDs), suggesting that haploinsufficiency of CHRNA7, the gene that codes for the alpha 7 nicotinic acetylcholine receptor (alpha 7 nAChR) subunit, is an etiological mechanism. Independent of these genetic data, given the location of alpha 7 nAChRs on gamma-aminobutyric acid-inhibitory neurons and their role in maintaining central inhibitory tone, a compelling pharmacological rationale exists for therapeutically targeting the alpha 7 nAChR in persons with ASDs. Given the availability of positive allosteric modulators of nicotinic acetylcholine receptors and selective agonists for the alpha 7 nAChR (eg, choline derived from dietary administration of cytidine 5'diphosphocholine and anabasine derivatives), it is possible to conduct proof of concept'' clinical trials, exploring the effects of alpha 7 nAChR agonist interventional strategies on domains of psychopathology, such as attention, cognition, and memory, in persons with ASDs.
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