It is now established that the genetic architecture of schizophrenia involves rare, common and de novo risk alleles distributed across a large number of genes. Despite substantial genetic heterogeneity, different classes of mutation have been shown to converge onto common biological pathways,

implicating neuronal calcium signalling, components of the post synaptic density, synaptic plasticity, epigenetic regulation and the immune system in the disorder. It has also become clear that schizophrenia shares risk alleles with other neuropsychiatric disorders, with evidence of a gradient of mutational severity with intellectual disability and schizophrenia at the most extreme and moderate ends of this spectrum, respectively [ 55]. It is inevitable that further increases in sample size in both GWAS and sequencing studies will identify additional risk alleles and whole-genome sequencing will allow for more complex types of genetic variation to be examined, while permitting http://www.selleckchem.com/products/epz015666.html selleck inhibitor the investigation of rare alleles in regulatory elements. The work at Cardiff University was funded by Medical Research Council (MRC) Centre (G0800509) and Program Grants (G0801418) and the European Community’s Seventh Framework Programme (HEALTH-F2-2010-241909 (Project EU-GEI)). Nothing declared. Papers of particular interest, published within the period of review, have been highlighted as:

• of special interest “
“Current Opinion in Behavioral Sciences 2015, 2:xx–yy This review comes from a themed issue Montelukast Sodium on Behavioral genetics 2015 Edited by William Davies and Laramie Duncan http://dx.doi.org/10.1016/j.cobeha.2014.07.002 2352-1546/Published by Elsevier Ltd. The microscopic roundworm, Caenorhabditis elegans, was handpicked by Sydney Brenner as the ideal organism for genetic dissection of the nervous system [1]. The appeal was its transparency, simple anatomy, short life cycle, ease of cultivation, and hermaphroditic mode of reproduction. After almost 50 years of random and targeted genetic lesions there is a vast library of mutant

lines that can be conveniently stored as frozen stocks – there are currently loss-of-function alleles available for over 2/3 of the 20,514 protein-coding genes, in most cases there are multiple alleles, including conditional and gain-of-function [2•]. In addition to its facile genetics and well-annotated genome, the worm’s 302 neurons are optically and genetically accessible and make the only known connectome [3]. Finally, there are a variety of platforms for tracking all the subtleties of behavior, which is remarkably plastic despite the reproducible connectivity of the nervous system [4•]. The first systematic study of learning was reported in 1990 [5] and since then paradigms have been developed for associative and non-associative learning and for short and long-term memory (reviewed in [6]). For each paradigm, forward and reverse genetic strategies have been used to uncover the underlying neural circuitry and molecular mechanisms.