Disturbed synaptic connectivity in schizophrenia: Convergence of genetic risk factors during neurodevelopment

被引:42
作者
Hayashi-Takagi, Akiko [1 ]
Sawa, Akira [1 ,2 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21287 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21287 USA
关键词
Schizophrenia; Susceptible pathway for schizophrenia; Synaptic connectivity; Glutamate; Synapse development; MINOR PHYSICAL ANOMALIES; DENDRITIC SPINE DENSITY; NITRIC-OXIDE SYNTHASE; CORTICAL PYRAMIDAL NEURONS; AMINO-ACID OXIDASE; PREFRONTAL CORTEX; D-SERINE; BRAIN-DEVELOPMENT; RECEPTOR HYPOFUNCTION; POSTSYNAPTIC DENSITY;
D O I
10.1016/j.brainresbull.2010.04.007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The pathological mechanisms underlying schizophrenia are unclear. Although genetic susceptibility factors for schizophrenia likely influence neurodevelopmental processes, the onset of the disease is in adolescence and young adulthood. Here we review recent literatures implicating neurodevelopmental deficits in schizophrenia and discuss how genetic factors are involved in the processes toward onset of the disease. We emphasize the importance of postnatal glutamate synapse development in the pathology of the disorder These genetic risk factors contribute to the process possibly in a synergistic manner. The notion of signal pathways involving more than one genetic factor is in accord with the multifactorial nature of schizophrenia (C) 2010 Published by Elsevier Inc.
引用
收藏
页码:140 / 146
页数:7
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