Abstract
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.
Highlights
Alzheimer’s disease (AD) is a form of dementia that most commonly affects older people and is characterized by progressive cognitive decline, which usually starts with a decrease in memory [1,2]
It was revealed through ultrastructure experiments on AD brain specimens that neurofibrillary tangles (NFTs) are primarily composed of paired helical filaments (PHFs), which are fibrils of approximately 10 nm in diameter that form pairs with a helical three-dimensional conformation and a regularly repeated pattern of almost 65 nm [61,62,63]
It is supposed that the downregulation of tau phosphatase(s) or the upregulation of tau kinase(s) in case of AD can cause abnormal phosphorylation of tau, even though both events might not be mutually exclusive cAMP-dependent protein kinase (PKA), It is supposed that the downregulation of tau phosphatase(s) or the upregulation of tau kinase(s) in case of AD can cause abnormal phosphorylation of tau, even though both events might not be mutually exclusive [58]. cAMP-dependent protein kinase (PKA), calcium/calmodulin-dependent kinase II (CaMK-II), cyclin-dependent kinase 5 (Cdk5) and glycogen synthase kinase 3β (GSK-3β) are the kinases that are predicted to have a substantial contribution to the phosphorylation of brain tau [89]
Summary
Alzheimer’s disease (AD) is a form of dementia that most commonly affects older people and is characterized by progressive cognitive decline, which usually starts with a decrease in memory [1,2]. Flavonoids are found to subdue the microglial activation, to mediate inflammatory processes in the central nervous system (CNS) [31], to possess potent anti-amyloidogenic, antidepressant effects [32], as well as to improve memory and learning ability [33]. These natural substances exhibit anti-inflammatory [34,35,36], neuroprotective [37,38], antiaging [39], and anticholinesterase [40] properties. This review aims to focus on the molecular mechanisms of plant-derived flavonoids to increase the survivability of neuronal cells in AD and to lower the risk of cellular degeneration
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