On the Physiological Relevance of Muscarinic Acetylcholine Receptors in Alzheimer's Disease
Authors: Koch, H. J.; Haas, S.; Jurgens, T.
Source: Current Medicinal Chemistry, Volume 12, Number 24, November 2005 , pp. 2915-2921(7)
Publisher: Bentham Science Publishers
Abstract:
The loss of cholinergic neurons, particularly in the forebrain, plays an important role in the pathophysiology of Alzheimer's disease (DAT). This concept has lead to the effective treatment of DAT by means of acetylcholine (Ach) esterase inhibitors. G-protein-coupled muscarinic acetylcholine receptors (mAchR) are classified in 5 subtypes, the M1 receptor stimulation and M2 inhibition being especially associated with cognitive skills. Modified cerebral muscarinic receptor profiles in patients with Alzheimer's disease in addition to loss of Ach releasing neurons help us to understand the pathophysiology of dementia and offer potential therapeutic approaches. Specific agonists and antagonists of muscarinic receptors are discussed as possible treatment options in DAT. Experimental results postulate a positive long lasting modulation of the pathological neuronal protein pattern in addition to their cholinomimetic effect.Keywords: muscarinic receptors; dementia; agonist; antagonist
Document Type: Review article
DOI: http://dx.doi.org/10.2174/092986705774454742
Affiliations: 1: Neurologische Universitatsklinik am Bezirksklinikum Regensburg, Universitatsstrasse 84, 93053 Regensburg, Germany.
Publication date: 2005-11-01
- Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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- In this Subject: Pharmacology
- By this author: Koch, H. J. ; Haas, S. ; Jurgens, T.

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