Alzheimer’s Disease: Analysis of Flavonoids with Mechanism Focusing Upon Targeting Aβ- Deposition and BDNF/Trkb Along with Other Signalling Pathway

Abstract

Alzheimer's disease (AD) affects 60–70% of the global population and is one of the most common, severe, and progressive neurodegenerative illnesses in the elderly. Many signaling pathways are implicated in AD development, and while focusing on one pathway may reduce symptoms, it cannot offer a long-term solution. It has been discovered that using flavonoids to treat Alzheimer's disease is very beneficial. In addition, flavonoids have a variety of neuroprotective effects on the brain including defense of the brain against numerous neurotoxins and inhibition of the neuro-inflammatory process, as these actions will improve memory, learning, and other understandable. Plant parts such as berries, vegetables, roots, stems, flowers, and other sections include flavonoids, which are a group of naturally occurring chemicals with different phenolic structures. The flavonoid’s mechanism of action in AD involved the inhibition of acetylcholinesterase, butyryl cholinesterase, 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. Flavonoids communicate with different signalling pathways and adjust their activities, accordingly prompting valuable neuroprotective impacts. Flavonoids likewise hamper the movement of obsessive indications of neurodegenerative disorders by hindering neuronal apoptosis incited by neurotoxin substances. In this review, we briefly discussed about the classification of flavonoids and their neuroprotective properties that could be used as a potential source for the treatment of AD.  We also highlight the structural features of flavonoids.