TY - JOUR
T1 - Resveratrol and neuroprotection
T2 - an insight into prospective therapeutic approaches against Alzheimer’s disease from bench to bedside
AU - Islam, Fahadul
AU - Nafady, Mohamed H.
AU - Islam, Md Rezaul
AU - Saha, Susmita
AU - Rashid, Salma
AU - Akter, Aklima
AU - Harun-Or-Rashid, Md
AU - Akhtar, Muhammad Furqan
AU - Perveen, Asma
AU - Md. Ashraf, Ghulam
AU - Rahman, Md Habibur
AU - Hussein Sweilam, Sherouk
N1 - Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2022/7
Y1 - 2022/7
N2 - Alzheimer’s disease (AD) is the most common cause of dementia and cognitive impairment; yet, there is currently no treatment. A buildup of Aβ, tau protein phosphorylation, oxidative stress, and inflammation in AD is pathogenic. The accumulation of amyloid-beta (Aβ) peptides in these neurocognitive areas is a significant characteristic of the disease. Therefore, inhibiting Aβ peptide aggregation has been proposed as the critical therapeutic approach for AD treatment. Resveratrol has been demonstrated in multiple studies to have a neuroprotective, anti-inflammatory, and antioxidant characteristic and the ability to minimize Aβ peptides aggregation and toxicity in the hippocampus of Alzheimer’s patients, stimulating neurogenesis and inhibiting hippocampal degeneration. Furthermore, resveratrol’s antioxidant effect promotes neuronal development by activating the silent information regulator-1 (SIRT1), which can protect against the detrimental effects of oxidative stress. Resveratrol-induced SIRT1 activation is becoming more crucial in developing novel therapeutic options for AD and other diseases that have neurodegenerative characteristics. This review highlighted a better knowledge of resveratrol’s mechanism of action and its promising therapeutic efficacy in treating AD. We also highlighted the therapeutic potential of resveratrol as an AD therapeutic agent, which is effective against neurodegenerative disorders.
AB - Alzheimer’s disease (AD) is the most common cause of dementia and cognitive impairment; yet, there is currently no treatment. A buildup of Aβ, tau protein phosphorylation, oxidative stress, and inflammation in AD is pathogenic. The accumulation of amyloid-beta (Aβ) peptides in these neurocognitive areas is a significant characteristic of the disease. Therefore, inhibiting Aβ peptide aggregation has been proposed as the critical therapeutic approach for AD treatment. Resveratrol has been demonstrated in multiple studies to have a neuroprotective, anti-inflammatory, and antioxidant characteristic and the ability to minimize Aβ peptides aggregation and toxicity in the hippocampus of Alzheimer’s patients, stimulating neurogenesis and inhibiting hippocampal degeneration. Furthermore, resveratrol’s antioxidant effect promotes neuronal development by activating the silent information regulator-1 (SIRT1), which can protect against the detrimental effects of oxidative stress. Resveratrol-induced SIRT1 activation is becoming more crucial in developing novel therapeutic options for AD and other diseases that have neurodegenerative characteristics. This review highlighted a better knowledge of resveratrol’s mechanism of action and its promising therapeutic efficacy in treating AD. We also highlighted the therapeutic potential of resveratrol as an AD therapeutic agent, which is effective against neurodegenerative disorders.
KW - Alzheimer’s disease
KW - Autophagy induction
KW - Neuroinflammation
KW - Oxidative stress
KW - Resveratrol
KW - SIRT1
UR - http://www.scopus.com/inward/record.url?scp=85129884744&partnerID=8YFLogxK
U2 - 10.1007/s12035-022-02859-7
DO - 10.1007/s12035-022-02859-7
M3 - Review article
C2 - 35545730
AN - SCOPUS:85129884744
SN - 0893-7648
VL - 59
SP - 4384
EP - 4404
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 7
ER -