TY - JOUR
T1 - Better understanding of mechanisms of schizophrenia and bipolar disorder
T2 - From human gene expression profiles to mouse models
AU - Lin, Chi Ying
AU - Sawa, Akira
AU - Jaaro-Peled, Hanna
N1 - Funding Information:
We thank Yukiko L. Lema for organizing the manuscript and preparing the figure. We also thank Dr. Minae Niwa and Ms. Ashley Wilson for critical reading. Grant supports: from MH-084018 Silvo O. Conte Center (A.S.), MH-069853 (A.S.), MH-085226 (A.S.), MH-088753 (A.S.), Stanley (A.S.), RUSK (A.S.), S-R Foundations (A.S.), NARSAD (H.J-P., A.S.) and Maryland Stem Cell Research Fund (A.S.).
PY - 2012/1
Y1 - 2012/1
N2 - The molecular mechanisms of major mental illnesses, such as schizophrenia and bipolar disorder, are unclear. To address this fundamental question, many groups have studied molecular expression profiles in postmortem brains and other tissues from patients compared with those from normal controls. Development of unbiased high-throughput approaches, such as microarray, RNA-seq, and proteomics, have supported and facilitated this endeavor. In addition to genes directly involved in neuron/glia signaling, especially those encoding for synaptic proteins, genes for metabolic cascades are differentially expressed in the brains of patients with schizophrenia and bipolar disorder, compared with those from normal controls in DNA microarray studies. Here we propose the importance and usefulness of genetic mouse models in which such differentially expressed molecules are modulated. These animal models allow us to dissect the mechanisms of how such molecular changes in patient brains may play a role in neuronal circuitries and overall behavioral phenotypes. We also point out that models in which the metabolic genes are modified are obviously untested from mental illness viewpoints, suggesting the potential to re-address these models with behavioral assays and neurochemical assessments.
AB - The molecular mechanisms of major mental illnesses, such as schizophrenia and bipolar disorder, are unclear. To address this fundamental question, many groups have studied molecular expression profiles in postmortem brains and other tissues from patients compared with those from normal controls. Development of unbiased high-throughput approaches, such as microarray, RNA-seq, and proteomics, have supported and facilitated this endeavor. In addition to genes directly involved in neuron/glia signaling, especially those encoding for synaptic proteins, genes for metabolic cascades are differentially expressed in the brains of patients with schizophrenia and bipolar disorder, compared with those from normal controls in DNA microarray studies. Here we propose the importance and usefulness of genetic mouse models in which such differentially expressed molecules are modulated. These animal models allow us to dissect the mechanisms of how such molecular changes in patient brains may play a role in neuronal circuitries and overall behavioral phenotypes. We also point out that models in which the metabolic genes are modified are obviously untested from mental illness viewpoints, suggesting the potential to re-address these models with behavioral assays and neurochemical assessments.
KW - Bipolar disorder
KW - Gene expression
KW - Microarray
KW - Mouse models
KW - Schizophrenia
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U2 - 10.1016/j.nbd.2011.08.025
DO - 10.1016/j.nbd.2011.08.025
M3 - Review article
C2 - 21914480
AN - SCOPUS:81955167938
SN - 0969-9961
VL - 45
SP - 48
EP - 56
JO - Neurobiology of Disease
JF - Neurobiology of Disease
IS - 1
ER -