Cortical development and neuropathology in schizophrenia.
Cortical development and neuropathology in schizophrenia.
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DOI：
10.1002/9780470514795.ch14
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发表时间：
2007-09
期刊：
影响因子：
--
通讯作者：
E. Jones
中科院分区：
文献类型：
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作者：
E. Jones
流行病学研究表明，怀孕期间发生的扰动可增加后代患精神分裂症的发生率。对一些精神分裂症患者大脑的神经病理学检查表明，大脑皮层发育后期的缺陷，特别是神经元迁移和皮层连接模式的建立和完善的最后阶段，可能涉及。这些研究大多是推测性的，在连接前额叶皮层、基底前脑、丘脑中背侧和内侧颞叶皮层的回路中，原发性病变与潜在的继发性逆行和顺行效应之间的关系尚不清楚。基于神经形态学和基因表达研究，我们的假设是，在发育中的大脑皮层的亚板区，迁移障碍或预编程细胞死亡模式导致其上皮层无法建立正常的连接模式。这种受损的电路随后失代偿，导致精神分裂症症状和神经递质和受体相关分子基因表达改变的活动依赖性表现。
Epidemiological studies suggest that perturbations occurring during pregnancy can increase the incidence of schizophrenia among offspring. Examination of the neuropathology of the brains of some schizophrenics suggests that a defect in the later phases of cerebral cortical development, notably the last phases of neuronal migration and the establishment and refinement of patterns of cortical connections, may be involved. Most of these studies are conjectural, and the relationship between primary lesions and potential secondary retrograde and anterograde effects in the circuitry linking the prefrontal cortex, basal forebrain, mediodorsal thalamus and medial temporal cortex is unknown. Our hypothesis, based on neuromorphological and gene expression studies, is that a disturbance of migration or in the pattern of preprogrammed cell death in the subplate zone of the developing cerebral cortex causes a failure to establish normal patterns of connections in the overlying cortex. This compromised circuitry subsequently decompensates, leading to schizophrenic symptoms and activity-dependent manifestations of altered gene expression for neurotransmitter- and receptor-related molecules.