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Mitochondrial abnormalities in neurodegenerative models and possible interventions: Focus on Alzheimer's disease, Parkinson's disease, Huntington's disease.
Mitochondrion. 2020 11; 55:14-47.M

Abstract

Mitochondrial abnormalities in the brain are considered early pathological changes in neurogenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). The mitochondrial dysfunction in the brain can be induced by toxic proteins, including amyloid-beta (Aβ), phosphorylated tau, alpha-synuclein (α-syn) and mutant huntingtin (mtHTT). These proteins cause mitochondrial genome damage, increased oxidative stress, decreased mitochondrial membrane permeability, and diminished ATP production. Consequently, synaptic dysfunction, synaptic loss, neuronal apoptosis, and ultimately cognitive impairment are exhibited. Therefore, the restoration of mitochondrial abnormalities in the brain is an alternative intervention to delay the progression of neurodegenerative diseases in addition to reducing the level of toxic proteins, especially Aβ, and restored synaptic dysfunction by interventions. Here we comprehensively review mitochondrial alterations in the brain of neurodegenerative models, specifically AD, PD and HD, from both in vitro and in vivo studies. Additionally, the correlation between mitochondrial changes, cognitive function, and disease progression from in vivo studies is described. This review also summarizes interventions that possibly attenuate mitochondrial abnormalities in AD, PD and HD models from both in vitro and in vivo studies. This may lead to the introduction of novel therapies that target on brain mitochondria to delay the progression of AD, PD and HD.

Authors+Show Affiliations

Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai 50200, Thailand. Electronic address: siriporn.c@cmu.ac.th.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

32828969

Citation

Pantiya, Patcharapong, et al. "Mitochondrial Abnormalities in Neurodegenerative Models and Possible Interventions: Focus On Alzheimer's Disease, Parkinson's Disease, Huntington's Disease." Mitochondrion, vol. 55, 2020, pp. 14-47.
Pantiya P, Thonusin C, Chattipakorn N, et al. Mitochondrial abnormalities in neurodegenerative models and possible interventions: Focus on Alzheimer's disease, Parkinson's disease, Huntington's disease. Mitochondrion. 2020;55:14-47.
Pantiya, P., Thonusin, C., Chattipakorn, N., & Chattipakorn, S. C. (2020). Mitochondrial abnormalities in neurodegenerative models and possible interventions: Focus on Alzheimer's disease, Parkinson's disease, Huntington's disease. Mitochondrion, 55, 14-47. https://doi.org/10.1016/j.mito.2020.08.003
Pantiya P, et al. Mitochondrial Abnormalities in Neurodegenerative Models and Possible Interventions: Focus On Alzheimer's Disease, Parkinson's Disease, Huntington's Disease. Mitochondrion. 2020;55:14-47. PubMed PMID: 32828969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial abnormalities in neurodegenerative models and possible interventions: Focus on Alzheimer's disease, Parkinson's disease, Huntington's disease. AU - Pantiya,Patcharapong, AU - Thonusin,Chanisa, AU - Chattipakorn,Nipon, AU - Chattipakorn,Siriporn C, Y1 - 2020/08/20/ PY - 2020/04/04/received PY - 2020/05/22/revised PY - 2020/08/14/accepted PY - 2020/8/24/pubmed PY - 2021/5/5/medline PY - 2020/8/24/entrez KW - Aging KW - Brain KW - Cognition KW - Mitochondria KW - Neurodegenerative diseases SP - 14 EP - 47 JF - Mitochondrion JO - Mitochondrion VL - 55 N2 - Mitochondrial abnormalities in the brain are considered early pathological changes in neurogenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). The mitochondrial dysfunction in the brain can be induced by toxic proteins, including amyloid-beta (Aβ), phosphorylated tau, alpha-synuclein (α-syn) and mutant huntingtin (mtHTT). These proteins cause mitochondrial genome damage, increased oxidative stress, decreased mitochondrial membrane permeability, and diminished ATP production. Consequently, synaptic dysfunction, synaptic loss, neuronal apoptosis, and ultimately cognitive impairment are exhibited. Therefore, the restoration of mitochondrial abnormalities in the brain is an alternative intervention to delay the progression of neurodegenerative diseases in addition to reducing the level of toxic proteins, especially Aβ, and restored synaptic dysfunction by interventions. Here we comprehensively review mitochondrial alterations in the brain of neurodegenerative models, specifically AD, PD and HD, from both in vitro and in vivo studies. Additionally, the correlation between mitochondrial changes, cognitive function, and disease progression from in vivo studies is described. This review also summarizes interventions that possibly attenuate mitochondrial abnormalities in AD, PD and HD models from both in vitro and in vivo studies. This may lead to the introduction of novel therapies that target on brain mitochondria to delay the progression of AD, PD and HD. SN - 1872-8278 UR - https://www.unboundmedicine.com/medline/citation/32828969/Mitochondrial_abnormalities_in_neurodegenerative_models_and_possible_interventions:_Focus_on_Alzheimer's_disease_Parkinson's_disease_Huntington's_disease_ DB - PRIME DP - Unbound Medicine ER -