https: or or doi.org or 10.47739 or 2374-0124 or
- 1. Department of Psychiatry, Showa University, Japan
- 2. Tokyo Metropolitan, Tobu Medical Center, Japan
- 3. Department of Psychiatry, Showa University, Japan
- 4. Department of Anesthegiology, Juntendo University, Japan
- 5. Department of Clinical Psychopharmacy, Showa University, Japan
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