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Cited 67 time in webofscience Cited 78 time in scopus
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Antioxidant and Neuroprotective Effects of Caffeine against Alzheimer's and Parkinson's Disease: Insight into the Role of Nrf-2 and A2AR Signalingopen access

Authors
Ikram, MuhammadPark, Tae JuAli, TahirKim, Myeong Ok
Issue Date
Sep-2020
Publisher
MDPI
Keywords
caffeine; Alzheimer’ s disease; Parkinson’ s disease; neurodegeneration; neuroprotective effects; antioxidant effects
Citation
ANTIOXIDANTS, v.9, no.9, pp 1 - 21
Pages
21
Indexed
SCIE
SCOPUS
Journal Title
ANTIOXIDANTS
Volume
9
Number
9
Start Page
1
End Page
21
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/6229
DOI
10.3390/antiox9090902
ISSN
2076-3921
2076-3921
Abstract
This paper reviews the results of studies conducted on the role of caffeine in the management of different neurological disorders, such as Parkinson's disease (PD) and Alzheimer's disease (AD). To highlight the potential role of caffeine in managing different neurodegenerative diseases, we identified studies by searching PubMed, Web of Science, and Google Scholar by scrutinizing the lists of pertinent publications. According to the collected overall findings, caffeine may reduce the elevated oxidative stress; inhibit the activation of adenosine A2A, thereby regulating the accumulation of A beta; reduce the hyperphosphorylation of tau; and reduce the accumulation of misfolded proteins, such as alpha-synuclein, in Alzheimer's and Parkinson's diseases. The studies have suggested that caffeine has promising protective effects against different neurodegenerative diseases and that these effects may be used to tackle the neurological diseases and/or their consequences. Here, we review the ongoing research on the role of caffeine in the management of different neurodegenerative disorders, focusing on AD and PD. The current findings suggest that caffeine produces potent antioxidant, inflammatory, and anti-apoptotic effects against different models of neurodegenerative disease, including AD, PD, and other neurodegenerative disorders. Caffeine has shown strong antagonistic effects against the adenosine A2A receptor, which is a microglial receptor, and strong agonistic effects against nuclear-related factor-2 (Nrf-2), thereby regulating the cellular homeostasis at the brain by reducing oxidative stress, neuroinflammation, regulating the accumulation of alpha-synuclein in PD and tau hyperphosphorylation, amyloidogenesis, and synaptic deficits in AD, which are the cardinal features of these neurodegenerative diseases.
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