Mitochondrial dysfunction in neurodegenerative disorders: Potential therapeutic application of mitochondrial transfer to central nervous system-residing cells

Mitochondrial dysfunction is reiteratively involved in the pathogenesis of diverse neurodegenerative diseases. Current in vitro and in vivo approaches support that mitochondrial dysfunction is branded by several molecular and cellular defects, whose impact at different levels including the calcium and iron homeostasis, energetic balance and/or oxidative stress, makes it difficult to resolve them collectively given their multifactorial nature. Mitochondrial transfer offers an overall solution since it contains the replacement of damage mitochondria by healthy units. Therefore, this review provides an introducing view on the structure and energy-related functions of mitochondria as well as their dynamics. In turn, we summarize current knowledge on how these features are deregulated in different neurodegenerative diseases, including frontotemporal dementia, multiple sclerosis, amyotrophic lateral sclerosis, Friedreich ataxia, Alzheimer & PRIME;s disease, Parkinson & PRIME;s disease, and Huntington's disease. Finally, we analyzed current advances in mitochondrial transfer between diverse cell types that actively participate in neurodegenerative processes, and how they might be projected toward developing novel therapeutic strategies.

Automated summary

Mitochondrial dysfunction plays a significant role in the pathogenesis of various neurodegenerative diseases. The dysfunction is characterized by multiple molecular and cellular defects that affect calcium and iron homeostasis, energy balance, and oxidative stress. Mitochondrial transfer, which involves replacing damaged mitochondria with healthy ones, offers a potential solution. This review provides an overview of mitochondrial structure, energy-related functions, and dynamics, as well as the deregulation of these features in different neurodegenerative diseases.