Mitochondrial dysfunction in neurodegenerative disease

Mitochondrial dysfunction has emerged as a central feature of multiple neurodegenerative disorders including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. Recent advances in molecular biology have begun to elucidate the specific mechanisms by which mitochondrial impairment contributes to neuronal loss, including reactive oxygen species generation, calcium dyshomeostasis, and impaired mitophagy. The convergence of these pathways suggests common therapeutic targets across multiple disease entities.

This review summarizes recent findings on mitochondrial quality control mechanisms, with particular emphasis on the PINK1-Parkin pathway and its role in selective mitophagy. We discuss evidence from genetic, biochemical, and clinical studies supporting a causal role for mitochondrial dysfunction in disease pathogenesis. We further consider emerging therapeutic strategies aimed at restoring mitochondrial function, including small-molecule activators of mitochondrial biogenesis and gene therapy approaches targeting mitochondrial DNA mutations.

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