Ball M J, Fisman M, Hachinski V, Blume W, Fox A, Kral V A, Kirshen A J, Fox H, Merskey H
Lancet. 1985 Jan 5;1(8419):14-6. doi: 10.1016/s0140-6736(85)90965-1.
Preliminary data support the hypothesis that the decline of all higher cognitive functions in senile dementia of the Alzheimer type is attributable to histopathological changes in the hippocampal formation, with or without neocortical neuronal lesions. Previous literature amply supports the critical role of this "locus minoris resistentiae" in memory processing and cognitive physiology. New observations include quantitative morphometric evaluations of the hippocampal formation from a longitudinal study of prospectively tested patients and histological and neurochemical data from patients with a clinical presentation consistent with typical Alzheimer's disease, in whom the only neuropathological abnormality was devastating nerve cell loss and gliosis in the hippocampi.
阿尔茨海默型老年性痴呆中所有高级认知功能的衰退归因于海马结构的组织病理学变化，无论有无新皮质神经元损伤。先前的文献充分支持了这个“抵抗力较弱部位”在记忆处理和认知生理学中的关键作用。新的观察结果包括对前瞻性测试患者进行纵向研究时对海马结构的定量形态学评估，以及临床表现与典型阿尔茨海默病一致的患者的组织学和神经化学数据，这些患者唯一的神经病理学异常是海马中严重的神经细胞丢失和胶质增生。
