Emerging Signal Regulating Potential of Small Molecule Biflavonoids to Combat Neuropathological Insults of Alzheimer Disease

International audienceAlzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder which is linked with cognitive and memory impairment eventually can even lead to death. There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Aβ) plaques, and/or genetic as well as the environmental factors. Existing treatments can only provide symptomatic relief via providing temporary palliative therapy which can weaken the rate of AD-associated cognitive decline. Plants are the fundamental building blocks for the environment and produce various secondary metabolites. Biflavonoids are one among such secondary metabolite that possesses the potential to mediate noticeable change in the aggregation of Aβ and also efficiently can decrease the toxic effects of Aβ oligomers in comparison with the monoflavonoid moieties. Nevertheless, the molecular processes are yet to be well explained. However, flavonoids are found to cause a change in the Aβ and tau aggregation pathway to generate non-toxic aggregates. In this review, we have discussed the neuroprotective action of small molecule biflavonoid to reduce the neurodegenerative events of AD. Furthermore, this appraisal advances our knowledge to develop potential new targets for the treatment of AD