Mitochondrial Dysfunction and Oxidative Stress in Alzheimer's Disease

Mitochondria play a pivotal role in bioenergetics and respiratory functions, which are essential for the numerous biochemical processes underpinning cell viability. Mitochondrial morphology changes rapidly in response to external insults and changes in metabolic status via fission and fusion process...

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Bibliographic Details
Published in:Frontiers in aging neuroscience 2021-02, Vol.13, p.617588-617588
Main Authors: Misrani, Afzal, Tabassum, Sidra, Yang, Li
Format: Article
Language:English
Subjects:
Adenosine triphosphate
Alzheimer's disease
Antioxidants
Bioenergetics
Brain
By products
Calcium (mitochondrial)
Calcium homeostasis
Cell viability
Cytology
Deoxyribonucleic acid
DNA
Energy
fission
Free radicals
fusion
Homeostasis
Kinases
Lipid peroxidation
Lipids
Metabolism
Mitochondria
mitophagy
Neurodegeneration
Neurodegenerative diseases
Neuroscience
Oxidation
Oxidative stress
Pathogenesis
Phosphatase
Phosphorylation
Proteins
Reactive oxygen species
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Summary:Mitochondria play a pivotal role in bioenergetics and respiratory functions, which are essential for the numerous biochemical processes underpinning cell viability. Mitochondrial morphology changes rapidly in response to external insults and changes in metabolic status via fission and fusion processes (so-called mitochondrial dynamics) that maintain mitochondrial quality and homeostasis. Damaged mitochondria are removed by a process known as mitophagy, which involves their degradation by a specific autophagosomal pathway. Over the last few years, remarkable efforts have been made to investigate the impact on the pathogenesis of Alzheimer's disease (AD) of various forms of mitochondrial dysfunction, such as excessive reactive oxygen species (ROS) production, mitochondrial Ca dyshomeostasis, loss of ATP, and defects in mitochondrial dynamics and transport, and mitophagy. Recent research suggests that restoration of mitochondrial function by physical exercise, an antioxidant diet, or therapeutic approaches can delay the onset and slow the progression of AD. In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches.
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2021.617588