MITOCHONDRIAL DYSFUNCTION IN NEURODEGENERATIVE DISEASES: INSIGHTS INTO COMPLEX PATHWAYS

Abstract

Neurodegenerative diseases encompass a diverse range of disorders characterized by abnormal nervous system function arising from neuronal or myelin deficits. Prominent among these are Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Huntington's disease, each marked by distinct clinical manifestations, notably cognitive decline and motor impairment. As these ailments progress, symptoms exacerbate, and their prevalence escalates with advancing age. Despite their prevalence and impact, the intricate mechanisms underlying neurodegenerative diseases remain incompletely elucidated.

A pivotal focus in understanding these disorders involves the multifaceted organelles, mitochondria, which play a crucial role in powering essential neuronal functions. Mitochondria primarily contribute to cellular oxidative respiration, maintaining homeostasis through a delicate balance in both number and function. Disruptions in this equilibrium can be attributed to impaired glucose metabolism or perturbations in single-electron transport induced by genetic or exogenous factors. Such disruptions may result in abnormal functioning or reduced numbers of respiratory chain complexes within mitochondria. The consequence of these disturbances is the inhibition of electrochemical gradients, culminating in energy failure, a pivotal event in the onset and progression of neurodegenerative diseases.

This abstract seeks to provide an overview of the heterogeneity within neurodegenerative diseases, emphasizing the commonality in their clinical presentations, including cognitive decline and motor dysfunction. The age-related increase in their incidence underscores the pressing need for comprehensive understanding. The spotlight on mitochondria as central players in neurodegenerative mechanisms highlights the intricate relationship between energy homeostasis and disease pathogenesis. As this knowledge continues to evolve, it holds promise for innovative therapeutic approaches aimed at preserving mitochondrial function and ameliorating the impact of neurodegenerative diseases