Abstract
Mitochondrial dysfunction has emerged as a central pathological mechanism underlying a wide range of neurological disorders, including Alzheimer’s disease, Parkinson’s disease, stroke, and amyotrophic lateral sclerosis. As the primary source of cellular energy and a key regulator of metabolic homeostasis, mitochondria play a critical role in maintaining neuronal function and survival. Disruption of mitochondrial dynamics, bioenergetics, and signaling pathways leads to impaired energy production, increased oxidative stress, and activation of cell death pathways.
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