NDLI: Association study of a SNAP-25 microsatellite and attention deficit hyperactivity disorder.

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Association study of a SNAP-25 microsatellite and attention deficit hyperactivity disorder.

Content Provider	Semantic Scholar
Author	Mill, Jonathan Curran, Sarah Kent, Lindsey Huckett, Louise Richards, Sandra Taylor, Eric Asherson, Philip
Copyright Year	2002
Abstract	Several lines of evidence implicate synaptosomal-associated protein of 25 kDa (SNAP-25) in the etiology of attention deficit hyperactivity disorder (ADHD). Most notably, the coloboma mouse mutant, considered to be a good animal model of hyperactivity, has a deletion spanning this gene. Introducing a SNAP-25 transgene into these animals alleviates hyperlocomotion. We have identified a novel microsatellite repeat in SNAP-25 located between the 5'UTR and the first coding exon, and tested for association with ADHD. Case-control analyses suggest there may be a role of this polymorphism in ADHD, with one allele over-represented in controls and another over-represented in probands. Within-family tests of linkage and association confirmed these findings. Further work is needed to ascertain the role of SNAP-25 in ADHD and assess the functional significance of this polymorphism.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.epigenomicslab.com/wp-content/uploads/publications/Mill%20J%20et%20al.%20Association%20Study%20of%20a%20SNAP-25%20Microsatellite%20.pdf
Alternate Webpage(s)	https://www.epigenomicslab.com/wp-content/uploads/publications/Mill%20J%20et%20al.%20Association%20Study%20of%20a%20SNAP-25%20Microsatellite%20.pdf
PubMed reference number	11920846v1
Volume Number	114
Issue Number	3
Journal	American journal of medical genetics
Language	English
Access Restriction	Open
Subject Keyword	5' Untranslated Regions Attention deficit hyperactivity disorder Congenital ocular coloboma (disorder) Deletion Mutation Hyperactive behavior Movement Disorders Short Tandem Repeat Transgenes genetic linkage
Content Type	Text
Resource Type	Article

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