Neuropharmacology of Cevimeline and Muscarinic Drugs-Focus on Cognition and Neurodegeneration
Patrik Oleksak1, Michal Novotny2, Jiri Patocka3,4
1Department of Chemistry, Faculty of Science, University of Hradec Kralove, 50003 Hradec Kralove, Czech Republic.
Abstract:
At present, Alzheimer's disease (AD) and related dementias cannot be cured. Therefore, scientists all over the world are trying to find a new approach to prolong an active life of patients with initial dementia. Both pharmacological and non-pharmacological pathways are investigated to improve the key symptom of the disease, memory loss. In this respect, influencing the neuromodulator acetylcholine via muscarinic receptors, such as cevimeline, might be one of the therapeutic alternatives. The purpose of this study is to explore the potential of cevimeline on the cognitive functions of AD patients. The methodology is based on a systematic literature review of available studies found in Web of Science, PubMed, Springer, and Scopus on the research topic. The findings indicate that cevimeline has shown an improvement in experimentally induced cognitive deficits in animal models. Furthermore, it has demonstrated to positively influence tau pathology and reduce the levels of amyloid-β (Aβ) peptide in the cerebral spinal fluid of Alzheimer's patients. Although this drug has not been approved by the FDA for its use among AD patients and there is a lack of clinical studies confirming and extending this finding, cevimeline might represent a breakthrough in the treatment of AD.
Insights
Cevimeline shows promise for Alzheimer's disease (AD) treatment by improving cognitive deficits in animal models and potentially reducing amyloid-beta and tau pathologies in patients. Further clinical studies are needed to confirm its efficacy for dementia.
Area of Science:
- Neuroscience
- Pharmacology
- Gerontology
Background:
- Alzheimer's disease (AD) and related dementias are currently incurable, necessitating novel therapeutic strategies.
- Improving cognitive function, particularly memory loss, is a primary goal in managing early-stage dementia.
- Targeting the neuromodulator acetylcholine via muscarinic receptors presents a potential therapeutic avenue.
Purpose of the Study:
- To systematically review the potential of cevimeline in enhancing cognitive functions for patients with Alzheimer's disease.
- To explore cevimeline's impact on key pathological markers associated with AD.
Main Methods:
- A systematic literature review was conducted using major scientific databases: Web of Science, PubMed, Springer, and Scopus.
- Studies investigating cevimeline's effects on cognitive function and AD pathology were analyzed.
Main Results:
- Cevimeline demonstrated efficacy in improving experimentally induced cognitive deficits in animal models.
- The drug showed a positive influence on tau pathology and reduced amyloid-beta (Aβ) peptide levels in cerebrospinal fluid of AD patients.
Conclusions:
- Cevimeline exhibits potential as a therapeutic agent for Alzheimer's disease, impacting cognitive function and core pathologies.
- Despite promising preclinical and preliminary findings, FDA approval is pending, and extensive clinical trials are required to validate its use in AD patients.
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