Mitochondrial dysfunction and nitric oxide in Parkinson’s disease

Abstract

Mitochondrial dysfunction and nitric oxide (NO) dysregulation are considered to be one of the main molecular mechanisms in neurodegenerative disorders. Genetic mutations, such as SNCA, LRRK2, PINK1, and others, disrupt mitochondrial structure and function, leading to progressive neuronal damage. Excessive NO activity leads to increased oxidative stress, mitochondrial blockade, and neuronal tissue damage. Understanding these mechanisms will deepen our knowledge of pathogenesis and lay the foundation for the development of new therapeutic approaches. Future studies will aim to restore mitochondrial balance and halt neurodegeneration through targeted interventions.