Repository of Research and Investigative Information

Repository of Research and Investigative Information

Baqiyatallah University of Medical Sciences

Role of green tea catechins in prevention of age-related cognitive decline: Pharmacological targets and clinical perspective

(2019) Role of green tea catechins in prevention of age-related cognitive decline: Pharmacological targets and clinical perspective. Journal of Cellular Physiology. pp. 2447-2459. ISSN 0021-9541

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Abstract

Over the past decade, a wide range of scientific investigations have been performed to reveal neuropathological aspects of cognitive disorders; however, only limited therapeutic approaches currently exist. The failures of conventional therapeutic options as well as the predicted dramatic rise in the prevalence of cognitive decline in the coming future show the necessity for novel therapeutic agents. Recently, a wide range of research has focused on pharmacological activities of green tea catechins worldwide. Current investigations have clarified mechanistic effects of the catechins in inflammatory cascades, oxidative damages, different cellular transcription as well as transduction pathway in various body systems. It has been demonstrated that green tea polyphenols prevent age-related neurodegeneration through improvement of endogenous antioxidant defense mechanisms, modulation of neural growth factors, attenuation of neuroinflammatory pathway, and regulation of apoptosis. The catechins exhibited beneficial effects in cellular and animal models of neurodegenerative diseases including Alzheimer's disease, MS, and Parkinson's disease. The present review discusses the current pharmacological targets, which can be involved in the treatment of cognitive decline and addresses the action of catechin derivatives elicited from green tea on the multiple neural targets.

Item Type: Article
Keywords: Alzheimer disease catechins cognitive decline dementia green tea neurodegenerative disease phenolic compounds polyphenols 5-ht6 receptor antagonists n-terminal kinase alzheimers-disease epigallocatechin-3-gallate egcg acetylcholinesterase activity parkinsons-disease metabolic syndrome induced impairment vascular dementia oxidative stress Cell Biology Physiology
Divisions:
Page Range: pp. 2447-2459
Journal or Publication Title: Journal of Cellular Physiology
Journal Index: ISI
Volume: 234
Number: 3
Identification Number: https://doi.org/10.1002/jcp.27289
ISSN: 0021-9541
Depositing User: مهندس مهدی شریفی
URI: http://eprints.bmsu.ac.ir/id/eprint/2696

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