Torack R M
Neurosurgery. 1979 May;4(5):434-42. doi: 10.1227/00006123-197905000-00011.
The historical events in the evolution of Alzheimer's disease are reviewed, including the initial description by Alois Alzheimer and the subsequent controversy regarding the nosological specificity of this entity. The similarity of senile dementia and Alzheimer's disease is emphasized. The basis for the modern concept of Alzheimer's disease as premature or accelerated aging is included in the review. The pathological correlates of the major categories of adult dementia have been described. The traditional criteria of neurofibrillary tangles and senile plaques have been re-evaluated using the current insight into these changes afforded by electron microscopy and biochemistry. The significance of amyloid has been described because it occurs within the senile plaque and also as the essential component of congophilic angiopathy. The new information regarding neuronal cell counts and the loss of choline acetyltransferase has been evaluated in terms of an indication of a pathogenic mechanism of Alzheimer's disease. The current understanding of normal pressure hydrocephalus, Creutzfeldt-Jakob disease, and multi-infarct dementia has been described. Brain biopsy in dementia has been described as having diagnostic, research, pathogenic, and prognostic value. The precautions involving the performance and handling of the biopsy have been stressed, particularly because these procedures involve conditions of possible slow virus etiology. The polemic for Alzheimer's disease as aging or slow virus infection has been summarized. At this time a consideration seems justified that Alzheimer's disease is an age-related, slow virus disease due to a hitherto unknown immune defect. Aging as an etiological agent must be clarified before Alzheimer's disease, in any form, can be considered to be an inevitable consequence of longevity.
回顾了阿尔茨海默病演变过程中的历史事件，包括阿洛伊斯·阿尔茨海默的最初描述以及随后关于该实体疾病分类特异性的争议。强调了老年痴呆症与阿尔茨海默病的相似性。该综述还纳入了将阿尔茨海默病视为过早或加速衰老的现代概念的依据。描述了成人痴呆主要类型的病理相关因素。利用电子显微镜和生物化学对这些变化的当前认识，重新评估了神经纤维缠结和老年斑的传统标准。描述了淀粉样蛋白的意义，因为它存在于老年斑中，也是嗜刚果血管病的主要成分。根据阿尔茨海默病致病机制的指标，评估了关于神经元细胞计数和胆碱乙酰转移酶丧失的新信息。描述了目前对正常压力脑积水、克雅氏病和多发性梗死性痴呆的认识。痴呆症的脑活检已被描述为具有诊断、研究、致病和预后价值。强调了活检操作和处理中的注意事项，特别是因为这些程序涉及可能由慢病毒病因引起的情况。总结了关于阿尔茨海默病是衰老还是慢病毒感染的争论。此时，有理由认为阿尔茨海默病是一种与年龄相关的慢病毒疾病，是由于迄今未知的免疫缺陷所致。在阿尔茨海默病以任何形式被视为长寿的必然结果之前，必须先澄清衰老作为病因的问题。
