title: [Proposal of endogenous anticholinergic hypothesis in Alzheimer disease].
abstract: We previously speculated that anticholinergic activity (AA) endogenously appeared in Alzheimer's disease (AD) and accelerated AD pathology. In this article we introduce manuscripts supporting the endogenous appearance of AA in AD and the acceleration of AD pathology. We speculate that acethylcholine (ACh) not only is related to cognitive functions but also regulates the inflammatory system. Therefore in AD, in which the ACh system is down-regulated, the hyperactivity of the inflammatory system may be caused and among cyctokines, substances having anticholinergic properties may appear. We also refer to a case in which serum anticholinergic activity (SAA) disappeared with the prescription of memantine (an antidementia agent that has the property of the N-methyl-D-aspartate (NMDA) receptor blocker) and speculate that because the hyperactivity of the inflammatory system occurs by way of the hyperactivity of NMDA receptor, memantine could abolish the AA.
authors: Koji
authors: K
authors: Hori
authors: Kimiko
authors: K
authors: Konishi
authors: Ryo
authors: R
authors: Akita
authors: Masayuki
authors: M
authors: Tani
authors: Hiroi
authors: H
authors: Tomioka
authors: Yuka
authors: Y
authors: Kitajima
authors: Sachiko
authors: S
authors: Yokoyama
authors: Kazunari
authors: K
authors: Azuma
authors: Daisuke
authors: D
authors: Ikuse
authors: Norinao
authors: N
authors: Akashi
authors: Hajime
authors: H
authors: Yuda
authors: Mitsugu
authors: M
authors: Hachisu
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000473:pathology; D000818:Animals; D018680:Cholinergic Antagonists / Q000627:therapeutic use*; D006801:Humans; D008559:Memantine / Q000627:therapeutic use*; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects* / Q000378:metabolism
chemical_list: D018680:Cholinergic Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D000109:Acetylcholine; D008559:Memantine