Egan M F, Weinberger D R
Clinical Research Services, National Institute of Mental Health, Neuroscience Research Center at St. Elizabeths, Washington, D.C. 20032, USA.
Curr Opin Neurobiol. 1997 Oct;7(5):701-7. doi: 10.1016/s0959-4388(97)80092-x.
Schizophrenia appears to be a neurodevelopmental disorder involving dysfunctional prefrontal and temporal cortical neural systems. Recent data implicate presynaptic changes in subcortical dopamine neurotransmission, as well as alterations in cortical glutamatergic and GABAergic systems. Functional neuroimaging studies, combined with tests of neuropsychological function, suggest that cortical abnormalities underlie the cognitive deficits associated with schizophrenia. These deficits appear to account for much of the psychosocial dysfunction of schizophrenia and are particularly treatment refractory. Genetic studies have implicated several minor susceptibility loci; however, the clinical impact of these loci on the neurobiology of schizophrenia is still unclear. The use of neurobiological traits as phenotypes, such as cognitive deficits and cortical abnormalities, in genetic linkage studies may facilitate the identification of loci that underlie the most debilitating features of schizophrenia.
精神分裂症似乎是一种神经发育障碍，涉及前额叶和颞叶皮质神经功能系统的功能失调。最近的数据表明，皮质下多巴胺神经传递存在突触前变化，以及皮质谷氨酸能和γ-氨基丁酸能系统的改变。功能性神经影像学研究与神经心理功能测试相结合，表明皮质异常是精神分裂症相关认知缺陷的基础。这些缺陷似乎是精神分裂症社会心理功能障碍的主要原因，而且特别难以治疗。遗传学研究已经发现了几个次要的易感基因座；然而，这些基因座对精神分裂症神经生物学的临床影响仍不清楚。在基因连锁研究中使用神经生物学特征作为表型，如认知缺陷和皮质异常，可能有助于识别构成精神分裂症最具致残性特征基础的基因座。
