Braak H, Braak E, Bohl J
Department of Anatomy, J.W. Goethe University, Frankfurt, FRG.
Eur Neurol. 1993;33(6):403-8. doi: 10.1159/000116984.
The gradual intraneuronal accumulation of an insoluble fibrous material which partly consists of abnormally phosphorylated tau protein (neurofibrillary change) represents an important neuropathological hallmark of Alzheimer's disease. Neurofibrillary tangles and neuropil threads formed from this material develop in only a few types of cortical pyramidal cells. The first changes are seen in the entorhinal cortex. The destructive process then spreads into the hippocampal formation and eventually encroaches upon the isocortex. This sequence of events permits the distinction of six stages with a progressive increase in the severity of cortical destruction. The entorhinal region serves as an important interface between the isocortex and hippocampus. This interface function is markedly impaired due to the early deterioration of the entorhinal cortex. Severe entorhinal involvement is considered to represent the morphological counterpart of clinically incipient Alzheimer's disease. Similar changes are found in mentally impaired individuals suffering from Parkinson's disease or progressive supranuclear palsy.
一种不溶性纤维物质在神经元内逐渐积累，该物质部分由异常磷酸化的tau蛋白组成（神经原纤维变化），这是阿尔茨海默病重要的神经病理学标志。由这种物质形成的神经原纤维缠结和神经毡丝仅在少数几种皮质锥体细胞中出现。最初的变化见于内嗅皮质。随后破坏过程扩散至海马结构，最终侵犯同型皮质。这一系列事件使得能够区分六个阶段，皮质破坏的严重程度逐渐增加。内嗅区是同型皮质和海马之间的重要界面。由于内嗅皮质的早期退化，这种界面功能明显受损。严重的内嗅区受累被认为是临床早期阿尔茨海默病的形态学对应表现。在患有帕金森病或进行性核上性麻痹的精神受损个体中也发现了类似变化。
