Ball M J
Arch Pathol Lab Med. 1982 Apr;106(4):157-62.
The gray matter of patients dying of senile dementia of the Alzheimer type (SDAT) displays severe histopathologic lesions, including neurofibrillary tangles, neuritic (senile) plaques, granulovacuolar degeneration, Hirano bodies, and loss of nerve cells. The differences between the changes seen in SDAT and those seen in normal aging of the brain are quantitative. Results of neurochemical studies suggest that cholinergic neurons are especially afflicted, but clinical trials administering choline precursors in patients' food hve thus far been unsuccessful. Theories of its cause include genetic predisposition, an exogenous toxin, and a slow (latent) viral agent. No fully satisfactory animal model exists for this disorder, so prospective clinicopathologic investigations using tissues harvested at the time of autopsy may help elucidate the pathogenesis of this, the most common form of organic dementia.
死于阿尔茨海默型老年痴呆症（SDSDSD SDAT）的患者灰质呈现出严重的组织病理学病变，包括神经原纤维缠结、神经炎（老年）斑、颗粒空泡变性、 Hirano小体以及神经细胞缺失。SDAT中所见变化与正常脑老化中所见变化的差异是数量上的。神经化学研究结果表明胆碱能神经元尤其受累，但迄今为止在患者食物中给予胆碱前体的临床试验均未成功。其病因理论包括遗传易感性、外源性毒素和慢（潜伏）病毒因子。目前尚无针对这种疾病的完全令人满意的动物模型，因此使用尸检时采集的组织进行前瞻性临床病理研究可能有助于阐明这种最常见的器质性痴呆形式的发病机制。
