The Neuroprotective Potentiality of Flavonoids on Alzheimer's Disease

Int J Mol Sci. 2022 Nov 27;23(23):14835. doi: 10.3390/ijms232314835.

Abstract

Alzheimer's disease (AD), due to its spread, has become a global health priority, and is characterized by senile dementia and progressive disability. The main cause of AD and other neurodegenerations (Huntington, Parkinson, Amyotrophic Lateral Sclerosis) are aggregated protein accumulation and oxidative damage. Recent research on secondary metabolites of plants such as polyphenols demonstrated that they may slow the progression of AD. The flavonoids' mechanism of action in AD involved the inhibition of acetylcholinesterase, butyrylcholinesterase, Tau protein aggregation, β-secretase, oxidative stress, inflammation, and apoptosis through modulation of signaling pathways which are implicated in cognitive and neuroprotective functions, such as ERK, PI3-kinase/Akt, NFKB, MAPKs, and endogenous antioxidant enzymatic systems. This review focuses on flavonoids and their role in AD, in terms of therapeutic potentiality for human health, antioxidant potential, and specific AD molecular targets.

Keywords: apigenin; cyanidin 3-o-glucoside; epicatechin-3-gallate; flavonoids; genistein; gossypetin; myricetin; naringenin; neuroprotection; quercetin.

Publication types

  • Review

MeSH terms

  • Acetylcholinesterase / metabolism
  • Alzheimer Disease* / drug therapy
  • Alzheimer Disease* / metabolism
  • Amyloid Precursor Protein Secretases / metabolism
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use
  • Butyrylcholinesterase / metabolism
  • Flavonoids / pharmacology
  • Flavonoids / therapeutic use
  • Humans
  • Neuroprotective Agents* / pharmacology
  • Neuroprotective Agents* / therapeutic use

Substances

  • Butyrylcholinesterase
  • Flavonoids
  • Acetylcholinesterase
  • Amyloid Precursor Protein Secretases
  • Antioxidants
  • Neuroprotective Agents

Grants and funding

This research received no external funding.