Young J K
Department of Anatomy, Howard University, Washington DC 20059.
Med Hypotheses. 1992 May;38(1):1-4. doi: 10.1016/0306-9877(92)90151-2.
Considerable evidence suggests that in Alzheimer's disease, olfactory bulb damage may be a primary factor, causing degeneration and neurofibrillary tangles primarily in neurons connected with this brain area. Also, deposits of amyloid may involve an improper regulation of the cleavage of a precursor protein by glia. Finally, toxic effects of aluminium may be an etiological factor. This review proposes that all these seemingly unrelated aspects of Alzheimer's disease could be related to a disturbed function of metal-containing glia. Such a disturbance, initiated by or aggravating toxic effects of aluminum, may underlie initial damage in the olfactory bulb and/or other brain areas with a weakened blood-brain barrier and may be responsible for amyloid deposition.
大量证据表明,在阿尔茨海默病中,嗅球损伤可能是一个主要因素,主要导致与该脑区相连的神经元发生退化和神经原纤维缠结。此外,淀粉样蛋白沉积可能涉及胶质细胞对前体蛋白切割的调节不当。最后,铝的毒性作用可能是一个病因。本综述提出,阿尔茨海默病所有这些看似不相关的方面可能都与含金属胶质细胞的功能紊乱有关。这种由铝的毒性作用引发或加剧的紊乱,可能是嗅球和/或其他血脑屏障较弱的脑区初始损伤的基础,并且可能是淀粉样蛋白沉积的原因。