west曾提示:早老性痴呆患者的斑块中存在硅铝可能属继发性钙不足。我们亦曾认为:斑块中铝和硅的浓缩物也许是继发性演变而来,并赞同Candg博士及其同事关于钙对老年人的重要性。我们假设慢性钙水平低下或钙流量频繁改变,增加了斑块形成和神经原纤维纷乱(NFT)的可能性,从而亦破坏了记忆力形成。根据假设我们进行了以下规定;(1)钙水平较高,反之则影响微管的集合/分解。(2)在老年性痴呆的阿尔茨海默型(SDAT)中NFTs可能表示微管集合发生紊乱。(3)微管 West had suggested: Alzheimer’s disease in patients with plaque may be secondary calcium deficiency. We have also argued that the concentrates of aluminum and silicon in the patches may have evolved from the secondary and agree with Dr. Candg and colleagues about the importance of calcium for the elderly. We hypothesized that chronic low calcium levels or frequent changes in calcium flux increased the likelihood of plaque formation and neurofibrillary disorders (NFT), thus undermining memory formation. Under the assumption that we have the following provisions: (1) higher calcium levels, and vice versa affect the collection / decomposition of microtubules. (2) NFTs in Alzheimer’s type (SDAT) of senile dementia may indicate that the microtubule assembly is disrupted. (3) microtubules