Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease

发病机制 老年斑 疾病 神经科学 阿尔茨海默病 β淀粉样蛋白 医学 化学 药理学 生物信息学 生物 免疫学 病理
作者
Md. Sahab Uddin,Md. Tanvir Kabir,Kamal Niaz,Philippe Jeandet,Christophe Clément,Bijo Mathew,Abdur Rauf,Kannan R. R. Rengasamy,Eduardo Sobarzo‐Sánchez,Ghulam Md Ashraf,Lotfi Aleya
出处
期刊:Molecules [Multidisciplinary Digital Publishing Institute]
卷期号:25 (6): 1267-1267 被引量:133
标识
DOI:10.3390/molecules25061267
摘要

Alzheimer's disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer's pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis.

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