Campbell A
Department of Community & Environmental Medicine, University of California, CA, USA.
Med Hypotheses. 2001 Mar;56(3):388-91. doi: 10.1054/mehy.2000.1212.
The function of the amyloid precursor protein (APP) and its product, beta-amyloid, (Abeta) is at present unknown. The deposition of Abeta in senile plaques as well as meningeal and cerebral vessels has led many researchers to discount the possibility of a beneficial protective function for the protein. Thus it is generally believed that the aberrant processing of APP leads to increased beta-amyloid secretion that in turn leads to subsequent plaque formation and Alzheimer's disease. Here, a hypothesis is presented that the protein may indeed be protective and that a potential role for beta amyloid in innate immunity may exist.
淀粉样前体蛋白（APP）及其产物β-淀粉样蛋白（Aβ）的功能目前尚不清楚。Aβ在老年斑以及脑膜和脑血管中的沉积使许多研究人员排除了该蛋白具有有益保护功能的可能性。因此，人们普遍认为APP的异常加工会导致β-淀粉样蛋白分泌增加，进而导致随后的斑块形成和阿尔茨海默病。在此，我们提出一个假说，即该蛋白可能确实具有保护作用，并且β淀粉样蛋白在先天免疫中可能存在潜在作用。
