Memantine Abolishes Anticholinergic Activity in Patient with Alzheimer's Disease at Moderate Stage
- Corresponding Author:
- Koji Hori
Department of Psychiatry
Showa University Northern Yokohama Hospital
35-1 Chigasakichuo, Tsuzukiku
E-mail: [email protected]
Received date: July 24, 2012; Accepted date: August 15, 2012; Published date: August 21, 2012
Citation: Hori K, Konishi K, Tomioka H, Minegishi G, Tani M, et al. (2012) Memantine Abolishes Anticholinergic Activity in Patient with Alzheimer’s Disease at Moderate Stage. J Alzheimers Dis Parkinsonism 2:108. doi:10.4172/2161-0460.1000108
Copyright: © 2012 Hori K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
We already reported that anticholinergic activity (AA) can occur endogenously in patients with Alzheimer’s disease (AD) at moderate stage. Since there is a possibility that AA might accelerate the pathologic changes of AD (amyloid plaques and tau protein), it is important to establish treatment for abolishing AA. We report a 76-year-old man with Alzheimer’s disease (AD) at moderate stage, whose serum anticholinergic activity (SAA) was positive when his memory disturbance, disorientation, apathy and aphasia were worsened. His SAA disappeared after 3 months of treatment with memantine, antidementia agent with N-methyl-D-aspartate (NMDA) receptor antagonist. At the same time his apathy and aphasia were ameliorated. We speculated that down-regulation of acetylcholine (ACh) caused the appearance of clinical symptoms and the hyperactivity of NMDA at moderate stage, that the hyperactivity of NMDA caused the up-regulation of inflammation, which caused AA and that the suppressions not only of the clinical symptoms and but also of the inflammation were thought to be caused by the down-regulation of NMDA receptor by memantine, which caused the ameliorations of some kinds of clinical symptoms and the disappearance of AA. We considered our patient supported previous hypothesis that AA is generated endogenously in AD, SAA was a biological marker for rapid progression of AD and memantine abolished AA in AD in moderate stage.