Arnold S E, Franz B R, Trojanowski J Q
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia 19104.
Neurobiol Aging. 1994 May-Jun;15(3):299-303. doi: 10.1016/0197-4580(94)90024-8.
Immunohistochemistry and conventional stains were used to examine the brains of 10 elderly patients with both schizophrenia and dementia to characterize the neuropathology of their cognitive deterioration. Control cases included five nondemented elderly patients with schizophrenia, five age-compatible Alzheimer's disease (AD) patients, and five neurologically normal elderly patients. Only one of the patients with schizophrenia and dementia had AD, another was diagnosed with adult polyglucosan body disease, and the others were devoid of neuropathology that could account for dementia. Quantitation of immunohistochemically detected neurofibrillary tangles and senile plaques revealed similarly low counts for the normal control group and both schizophrenia groups. Typically, the neuropathological causes of dementia can be identified in up to 95% of cases, with AD accounting for 50-60%. The unexpected lack of neuropathological findings to explain the cognitive deterioration in this group of elderly patients with schizophrenia prompts speculation about alternative etiologies.
采用免疫组织化学和传统染色方法对10例患有精神分裂症和痴呆症的老年患者的大脑进行检查，以表征其认知衰退的神经病理学特征。对照病例包括5例无痴呆的老年精神分裂症患者、5例年龄匹配的阿尔茨海默病（AD）患者和5例神经功能正常的老年患者。患有精神分裂症和痴呆症的患者中只有1例患有AD，另1例被诊断为成人多糖体病，其他患者没有可解释痴呆症的神经病理学改变。对免疫组织化学检测到的神经原纤维缠结和老年斑进行定量分析，结果显示正常对照组和两个精神分裂症组的计数同样较低。通常，在高达95%的病例中可以确定痴呆症的神经病理学病因，其中AD占50 - 60%。在这组患有精神分裂症的老年患者中，意外缺乏可解释认知衰退的神经病理学发现，这引发了对其他病因的猜测。
