Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by a decline in cognitive function and neuronal damage. Although the precise pathobiology of AD remains elusive, accumulating evidence suggests that mitochondrial dysfunction is one of the underlying causes of AD. Mutations in mitochondrial or nuclear DNA that encode mitochondrial components may cause mitochondrial dysfunction. In particular, the dysfunction of electron transport chain complexes, along with the interactions of mitochondrial pathological proteins are associated with mitochondrial dysfunction in AD. Mitochondrial dysfunction causes an imbalance in the production of reactive oxygen species, leading to oxidative stress (OS) and vice versa. Neuroinflammation is another potential contributory factor that induces mitochondrial dysfunction. Phytochemicals or other natural compounds have the potential to scavenge oxygen free radicals and enhance cellular antioxidant defense systems, thereby protecting against OS-mediated cellular damage. Phytochemicals can also modulate other cellular processes, including autophagy and mitochondrial biogenesis. Therefore, pharmacological intervention via neuroprotective phytochemicals can be a potential strategy to combat mitochondrial dysfunction as well as AD. This review focuses on the role of phytochemicals in mitigating mitochondrial dysfunction in the pathogenesis of AD.
Highlights
Several studies have demonstrated that mitochondrial dysfunction leads to several neurodegenerative diseases, including Alzheimer’s disease (AD) [1,2,3]
reactive oxygen species (ROS)·− ) may be the causative factor leading to defects in mitochondrial respiration and the development processes of the human brain that are accompanied by augmented ROS generation
An effective therapeutic strategy can be developed against AD by targeting mitochondrial proteins
Summary
Several studies have demonstrated that mitochondrial dysfunction leads to several neurodegenerative diseases, including Alzheimer’s disease (AD) [1,2,3]. AD shows common symptoms such as insanity and leads to a morbid state and death in the aged population [4] In both familial and sporadic patterns, AD is characterized by dual unique medical hallmarks: senile plaques formed via the extracellular accumulation of amyloid-β (Aβ) peptide and intracellular deposition of neurofibrillary tangles (NFTs) formed via hyperphosphorylation of tau proteins [5,6]. Aggregated Aβ peptides, H2 O2 -induced hydroxyl radical, and mitochondrial dysfunction caused by APP in AD may restrain in addition to pharmacological approaches using phytochemicals that preserve mitochondrial dynamics [16] Owing to their therapeutic capabilities, phytobioactive compounds have been deliberated as favorable beneficial agents for AD and age-related diseases [17]. The current review describes the underlying mechanisms of mitochondrial dysfunction in the pathogenesis of AD and discuss how phytochemicals may mitigate mitochondrial dysfunction
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