Journal
MITOCHONDRION
Volume 55, Issue -, Pages 14-47Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2020.08.003
Keywords
Brain; Mitochondria; Aging; Neurodegenerative diseases; Cognition
Categories
Funding
- National Research Council of Thailand, Thailand
- Teaching Assistant and Research Assistant (TARA) Scholarship, Chiang Mai University, Thailand
- Thailand Research Fund grants, Thailand [MRG6280014]
- Chiang Mai University Center of Excellence Award, Thailand
- NSTDA Research Chair grant from the National Science and Technology Development Agency Thailand, Thailand
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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 (A beta), phosphorylated tau, alpha-synuclein (alpha-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 A beta, and restored synaptic dysfunction by interventions. Here we comprehensively review mitochondrial al terations 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.
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