Molecules (Mar 2020)

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

  • 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

DOI
https://doi.org/10.3390/molecules25061267
Journal volume & issue
Vol. 25, no. 6
p. 1267

Abstract

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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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