Brion J P
Laboratoire d'Anatomie pathologique et de Microscopie électronique, Université libre de Bruxelles.
Bull Mem Acad R Med Belg. 1999;154(6 Pt 2):287-94.
Neurofibrillary tangles, a hallmark neuropathological lesion of Alzheimer's disease and of the other tauopathies, are composed of hyperphosphorylated tau proteins (a microtubule-associated protein) assembled in the form of abnormal filaments. Hyperphosphorylation of tau proteins appears to be an early phenomenom, preceding their aggregation into fibrillar structures. This hyperphosphorylation could result from changes in the activation of signalling cascades. Presenilins, and their mutations, could be responsible for these changes and, by their ability to interfere with APP metabolism, play a central role in the formation of both neurofibrillary tangles and A beta amyloid deposits.
神经原纤维缠结是阿尔茨海默病及其他tau蛋白病的标志性神经病理损伤，由以异常细丝形式组装的高度磷酸化tau蛋白（一种微管相关蛋白）组成。tau蛋白的高度磷酸化似乎是一种早期现象，先于其聚集成纤维状结构。这种高度磷酸化可能是信号级联激活变化的结果。早老素及其突变可能是这些变化的原因，并且通过其干扰APP代谢的能力，在神经原纤维缠结和Aβ淀粉样蛋白沉积的形成中起核心作用。
