Mitochondria play a crucial role in expediting the energy homeostasis under varying environmental conditions. As mitochondria are controllers of both energy production and apoptotic pathways, they are also distinctively involved in controlling the neuronal cell survival and/or death. Numerous factors are responsible for mitochondria to get degraded with aging and huge functional failures in mitochondria are also found to be associated with the commencement of numerous neurodegenerative conditions, including Alzheimer's disease (AD). A large number of existing literatures promote the pivotal role of mitochondrial damage and oxidative impairment in the pathogenesis of AD. Numerous mitochondria associated processes such as mitochondrial biogenesis, fission, fusion, mitophagy, transportation and bioenergetics are crucial for proper functioning of mitochondria but are reported to be defective in AD patients. Though, the knowledge on the precise and in-depth mechanisms of these actions is still in infancy. Based upon the outcome of various significant studies, mitochondria are also being considered as therapeutic targets for AD. Here, we review the current status of mitochondrial defects in AD and also summarize the possible role of these defects in the pathogenesis of AD. The various approaches for developing the mitochondria-targeted therapies are also discussed here in detail. Consequently, it is suggested that improving mitochondrial activity via pharmacological and/or non-pharmacological interventions could postpone the onset and slow the development of AD. Further research and consequences of ongoing clinical trials should extend our understanding and help to validate conclusions regarding the causation of AD.
Keywords: ATP; Alzheimer's disease; Mitochondria; Mitophagy; Neurodegeneration; Reactive oxygen species; Therapeutics.
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