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[突触连接减少对精神分裂症发病机制、临床表现及病程的意义]

[Significance of synaptic connectivity reduction for pathogenesis, clinical picture and course of schizophrenia].

作者信息

Rabe-Jabłońska Jolanta

机构信息

Kliniki Zaburzeń Afektywnych i Psychiatrii Młodziezy, Katedry Psychiatrii Uniwersytetu Medycznego w Łodzi.

出版信息

Psychiatr Pol. 2003 Nov-Dec;37(6):951-64.

Abstract

Synaptic connectivity disorders are significant in the pathogenesis of schizophrenia. Myelinization and abnormal function of oligodendroglia are the most important factors damaging synaptic connectivity. The main phase of the pathogenetic process leading to schizophrenia is the loss of synaptic connectivity below critical level, dependent on primary synaptic density (caused by genetic and perinatal factors), and on elimInation of synaptic connection during late adolescence and early adulthood. Various clinical pictures and courses of schizophrenia are related to various levels of synaptic density reduction. New imaging techniques (MRI, MTI, DTI) found many abnormalities in white matter--in myelin and oligodendroglia in schizophrenics. Actually, we don't know, whether these abnormalities are primary (caused by genetic factors) or secondary (caused by other factors, fox example by glutamatergic excitotoxicity of oligodendroglia).

摘要

突触连接障碍在精神分裂症的发病机制中具有重要意义。少突胶质细胞的髓鞘形成和功能异常是破坏突触连接的最重要因素。导致精神分裂症的致病过程的主要阶段是突触连接丧失至临界水平以下,这取决于初级突触密度(由遗传和围产期因素引起),以及在青春期后期和成年早期突触连接的消除。精神分裂症的各种临床表现和病程与突触密度降低的不同程度有关。新的成像技术(MRI、MTI、DTI)发现精神分裂症患者的白质——髓鞘和少突胶质细胞存在许多异常。实际上,我们不知道这些异常是原发性的(由遗传因素引起)还是继发性的(由其他因素引起,例如少突胶质细胞的谷氨酸能兴奋性毒性)。

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