Arnold S E
Laboratory of Cellular and Molecular Neuropathology, Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA.
Harv Rev Psychiatry. 2001 Mar-Apr;9(2):69-76. doi: 10.1080/10673220127882.
The neurobiological basis of cognitive and functional deterioration commonly observed in elderly persons with schizophrenia is unclear. Despite superficial similarities in the clinical and neuropsychological profiles of schizophrenia in late life with neurodegenerative dementias, extensive neuropathological investigations have failed to find any evidence of neurodegeneration or neural injury beyond what is typically observed in brains of individuals without neuropsychiatric illness. In contrast, growing neuropathological data indicate aberrant brain development and connectivity in schizophrenia (including abnormalities in cytoarchitecture, innervation, and synaptic integrity) and abnormal molecular signaling pathways important in the formation of the nervous system and ongoing plasticity in maturity. These developmental abnormalities may represent a state of decreased cerebral reserve that causes persons with schizophrenia to be more vulnerable to the toxic effects of even "normal" accumulations of age-related neurodegenerative lesions.
精神分裂症老年患者中常见的认知和功能衰退的神经生物学基础尚不清楚。尽管老年精神分裂症的临床和神经心理学特征与神经退行性痴呆有表面上的相似之处，但广泛的神经病理学研究未能发现任何神经退行性变或神经损伤的证据，超出了无神经精神疾病个体大脑中通常观察到的范围。相比之下，越来越多的神经病理学数据表明，精神分裂症存在大脑发育异常和连接异常（包括细胞结构、神经支配和突触完整性异常），以及在神经系统形成和成熟过程中持续可塑性方面重要的异常分子信号通路。这些发育异常可能代表一种脑储备减少的状态，使精神分裂症患者更容易受到与年龄相关的神经退行性病变即使是“正常”积累的毒性作用的影响。
