Why Does the Progression of Alzheimer’s disease Accelerate?

Abstract

We have already reported that anticholinergic activity (AA) appeared endogenously in Alzheimer’s disease (AD) serum, and may accelerate AD pathology. In this article we introduce the reasons for this. We comment on the roles of acetylcholine (Ach) downregulation and AA in AD, show two patterns of AD rapid progression associated with AA, and three putative patterns of amyloid pathology in AD. We speculate that ACh downregulation and AA may induce inflammatory hyperactivity in both the central nervous system and peripheral tissue, as well as among inflammatory cytokines that may have AA. This ACh downregulation in AD may extend the pathological processes in the central nervous system to peripheral tissues and vice versa, whereas AA in AD may be a final common pathway in the amyloid-producing process from various invasions. In addition, we discuss our proposed hypothesis of endogenous AA in AD and consider its implications. Therapeutically, we recommend that prescribing cholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists are appropriate for the “prevention” and “treatment” of rapid progression of AD respectively. In this context, it is important to prevent iatrogenic overdosing or polypharmacy for patients with AD. Furthermore, it is important to ensure that patients with AD are not suffering from concurrent physical illness or mental stress because this may facilitate the rapid progression of AD. Finally, we consider the limitations of the proposed hypothesis of the endogenous appearance of AA in AD

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Cite this paper

@inproceedings{Hori2014WhyDT, title={Why Does the Progression of Alzheimer’s disease Accelerate?}, author={Koji Hori and Kimiko Konishi and Masayuki Tani and Hiroi Tomioka and Ryo Akita and Yuka Kitajima and Mari Aoki and Nodoka Kikuchi and Daisuke Ikuse and Norihisa Akashi and Misa Hosoi and Koichi Jimbo and Mitsugu Hachisu}, year={2014} }