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

• Published in: Journal of translational medicine Vol. 21; no. 1; pp. 1 - 613
• Main Authors: Bustamante-Barrientos, Felipe A., Luque-Campos, Noymar, Araya, María Jesús, Lara-Barba, Eliana, de Solminihac, Javiera, Pradenas, Carolina, Molina, Luis, Herrera-Luna, Yeimi, Utreras-Mendoza, Yildy, Elizondo-Vega, Roberto, Vega-Letter, Ana María, Luz-Crawford, Patricia
• Format: Journal Article
• Language: English
• Published: London BioMed Central 09.09.2023; BMC
• Subjects: Alzheimer's disease; Amyotrophic lateral sclerosis; Ataxia; Autophagy; Calcium homeostasis; Central nervous system; Cognition & reasoning; Cytochrome; Dementia; Dementia disorders; Friedreich's ataxia; Frontotemporal dementia; Homeostasis; Huntingtons disease; Kinases; Membranes; Metabolism; Mitochondria; Multiple sclerosis; Neurodegenerative diseases; Oxidative stress; Proteins; Quality control; Review
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-023-04493-w

Abstract 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´s disease, Parkinson´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.