TY - JOUR
T1 - Mouse models of gene-environment interactions in schizophrenia
AU - Kannan, Geetha
AU - Sawa, Akira
AU - Pletnikov, Mikhail V.
N1 - Funding Information:
We thank the members of a collaborative study supported by the Conte Center at Johns Hopkins on gene–environmental interactions of cortical development and the pathology of schizophrenia. The authors are grateful to Joshua Crawford, MS for his editorial comments and suggestions. GK is supported by the Stanley Medical Research Institute (SMRI) and MH-094268 Silvo O. Conte Center grants. MVP is supported by MH-083728 and MH-094268 Silvo O. Conte Center grants, of the Brain and Behavior Research Foundation, SMRI ; AS is supported by NIH MH-084018 , MH-094268 , the Silvo O. Conte Center , MH-069853 , MH-085226 , MH-088753 , and MH-092443 , the SMRI, RUSK, and S-R foundations, the Brain and Behavior Research Foundation, and the Maryland Stem Cell Research Fund.
PY - 2013/9
Y1 - 2013/9
N2 - Gene-environment interactions (GEIs) likely play significant roles in the pathogenesis of schizophrenia and underlie differences in pathological, behavioral, and clinical presentations of the disease. Findings from epidemiology and psychiatric genetics have assisted in the generation of animal models of GEI relevant to schizophrenia. These models may provide a foundation for elucidating the molecular, cellular, and circuitry mechanisms that mediate GEI in schizophrenia. Here we critically review current mouse models of GEI related to schizophrenia, describe directions for their improvement, and propose endophenotypes to provide a more tangible basis for molecular studies of pathways of GEI and facilitate the identification of novel therapeutic targets.
AB - Gene-environment interactions (GEIs) likely play significant roles in the pathogenesis of schizophrenia and underlie differences in pathological, behavioral, and clinical presentations of the disease. Findings from epidemiology and psychiatric genetics have assisted in the generation of animal models of GEI relevant to schizophrenia. These models may provide a foundation for elucidating the molecular, cellular, and circuitry mechanisms that mediate GEI in schizophrenia. Here we critically review current mouse models of GEI related to schizophrenia, describe directions for their improvement, and propose endophenotypes to provide a more tangible basis for molecular studies of pathways of GEI and facilitate the identification of novel therapeutic targets.
KW - Animal models
KW - Endophenotypes
KW - Gene-environment interaction
KW - Schizophrenia
KW - Translational neuroscience
UR - http://www.scopus.com/inward/record.url?scp=84879782139&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84879782139&partnerID=8YFLogxK
U2 - 10.1016/j.nbd.2013.05.012
DO - 10.1016/j.nbd.2013.05.012
M3 - Review article
C2 - 23748077
AN - SCOPUS:84879782139
VL - 57
SP - 5
EP - 11
JO - Neurobiology of Disease
JF - Neurobiology of Disease
SN - 0969-9961
ER -