Journal
NEURAL REGENERATION RESEARCH
Volume 16, Issue 8, Pages 1467-1482Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.303007
Keywords
aging; Alzheimer's disease; amyotrophic lateral sclerosis; Huntington's disease; mitochondrial biogenesis; mitochondrial dysfunction; mtDNA mutations; neurodegeneration; oxidative stress; Parkinson's disease
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Funding
- European Regional Development Fund -Project MAGNET [CZ.02.1.01/0.0/0.0/15_003/0000492]
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Neurodegenerative diseases manifest distinct molecular mechanisms with abnormal protein dynamics and impaired bioenergetics. Mitochondrial dysfunction is a significant feature in their pathogenesis, yet effective treatment routes are currently lacking.
Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis are a heterogeneous group of debilitating disorders with multifactorial etiologies and pathogeneses that manifest distinct molecular mechanisms and clinical manifestations with abnormal protein dynamics and impaired bioenergetics. Mitochondrial dysfunction is emerging as an important feature in the etiopathogenesis of these age-related neurodegenerative diseases. The prevalence and incidence of these diseases is on the rise with the increasing global population and average lifespan. Although many therapeutic approaches have been tested, there are currently no effective treatment routes for the prevention or cure of these diseases. We present the current status of our knowledge and understanding of the involvement of mitochondrial dysfunction in these diseases and highlight recent advances in novel therapeutic strategies targeting neuronal bioenergetics as potential approach for treating these diseases.
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