Open AccessMore than the sum of its parts: new mouse models for dissecting the genetic complexities of Williams–Beuren syndrome
Author(s) -
MeyerLindenberg Andreas
Publication year - 2009
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.1002/emmm.200900007
Subject(s) - schizophrenia (object oriented programming) , genetic architecture , autism , williams syndrome , phenotype , bipolar disorder , population , genetics , biology , neuroscience , gene , bioinformatics , medicine , psychiatry , cognition , environmental health
Psychiatric disorders are a common, severe and disabling group of diseases where progress in finding novel molecular targets has been slow. This is partly due to our lack of understanding of the molecular pathophysiology of these conditions as they play out in the brain (Insel & Scolnick, 2006). Since many of these diseases (such as schizophrenia, bipolar disorder or autism) are highly heritable, a genetic approach to dissecting the risk architecture is a promising avenue for molecular medicine; however, variants in single genes frequently present in the population have only small to moderate effects on complex behavioural phenotypes (O'Donovan et al, 2008).