Mitochondrial dysfunction in neurodegenerative diseases: Mechanisms, consequences, and therapeutic interventions

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ID: 309433
2025
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Abstract
Mitochondria are critical regulators of neuronal survival, energy metabolism, calcium homeostasis, and apoptotic signaling. Dysfunctional mitochondria have emerged as a central feature in neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS). Impairments in oxidative phosphorylation, excessive reactive oxygen species (ROS) production, disrupted calcium handling, defective mitophagy, and altered mitochondrial dynamics collectively compromise neuronal function and viability. This review synthesizes current evidence on the mechanisms underlying mitochondrial dysfunction in neurodegeneration, highlighting disease-specific alterations in electron transport chain activity, mitochondrial bioenergetics, and quality control pathways. Furthermore, therapeutic strategies targeting mitochondria—including mitochondrial antioxidants, NAD⁺ precursors, mitophagy modulators, gene therapy, and mitochondrial biogenesis enhancers—are discussed in the context of emerging precision medicine approaches. Despite promising preclinical findings, challenges such as effective drug delivery across the blood–brain barrier, patient heterogeneity, and the need for reliable biomarkers remain. Advancements in mitochondrial imaging, multi-omics profiling, and patient-derived stem cell models offer opportunities for the development of personalized mitochondria-centered interventions aimed at mitigating neurodegenerative progression.
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Authors Olaide Kuburat Olanrewaju
Journal Aminu Kano Academic Scholars Association Multidisciplinary Journal
Year 2025
DOI
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URL
https://akasa.com.ng/ojs/index.php/journal/article/view/96
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