Mitochondrial dysfunction and oxidative stress in Alzheimer’s disease, and Parkinson’s disease, Huntington’s disease and Amyotrophic Lateral Sclerosis -An updated review

Jun 3, 2023Mitochondrion

Mitochondria problems and oxidative stress in Alzheimer’s, Parkinson’s, Huntington’s, and ALS – An updated review

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Abstract

Mitochondrial dysfunction is an early pathogenic mechanism associated with neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's, and Amyotrophic Lateral Sclerosis.

Misfolded proteins in the central nervous system may induce oxidative damage, contributing to neurodegeneration.
Oxidative stress and reduced mitochondrial activity are linked to the pathogenesis of Parkinson's disease.
Amyloid-ß and tau proteins are associated with mitochondrial malfunction, which may lead to Alzheimer's disease.
Huntington's disease is characterized by polyglutamine expansion, affecting mitochondrial function and leading to selective neurodegeneration.
Mitochondria play a crucial role in regulating energy utilization and calcium homeostasis in neurons, with dysfunction potentially preceding observable symptoms.

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Misfolded proteins in the central nervous system can induce oxidative damage, which can contribute to neurodegenerative diseases in the mitochondria. Neurodegenerative patients face early mitochondrial dysfunction, impacting energy utilization. Amyloid-ß and tau problems both have an effect on mitochondria, which leads to mitochondrial malfunction and, ultimately, the onset of Alzheimer's disease. Cellular oxygen interaction yields reactive oxygen species within mitochondria, initiating oxidative damage to mitochondrial constituents. Parkinson's disease, linked to oxidative stress, α-synuclein aggregation, and inflammation, results from reduced brain mitochondria activity. Mitochondrial dynamics profoundly influence cellular apoptosis via distinct causative mechanisms. The condition known as Huntington's disease is characterized by an expansion of polyglutamine, primarily impactingthe cerebral cortex and striatum. Research has identified mitochondrial failure as an early pathogenic mechanism contributing to HD's selective neurodegeneration. The mitochondria are organelles that exhibit dynamism by undergoing fragmentation and fusion processes to attain optimal bioenergetic efficiency. They can also be transported along microtubules and regulateintracellular calcium homeostasis through their interaction with the endoplasmic reticulum. Additionally, the mitochondria produce free radicals. The functions of eukaryotic cells, particularly in neurons, have significantly deviated from the traditionally assigned role of cellular energy production. Most of them areimpaired in HD, which may lead to neuronal dysfunction before symptoms manifest. This article summarizes the most important changes in mitochondrial dynamics that come from neurodegenerative diseases including Alzheimer's, Parkinson's, Huntington's and Amyotrophic Lateral Sclerosis. Finally, we discussed about novel techniques that can potentially treat mitochondrial malfunction and oxidative stress in four most dominating neuro disorders.

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Mitochondrial dysfunction and oxidative stress in Alzheimer’s disease, and Parkinson’s disease, Huntington’s disease and Amyotrophic Lateral Sclerosis -An updated review

Abstract

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