Oxidative Stress in DNA Damage and Neurodegenerative Diseases: Unveiling The Mechanisms and Therapeutic Opportunities

Oxidative stress is marked by disproportionate levels of reactive oxygen species (ROS) and antioxidant defenses and is a key factor in initiating DNA damage and neurodegenerative diseases. Increased reactive oxygen species (ROS) levels can lead to oxidative DNA lesions, disrupting cellular function and contributing to genomic instability. Oxidative stress is linked to neuronal degeneration, particularly in conditions such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD), where DNA damage accelerates the progression of these disorders. Hence, the importance of therapeutic measures to reduce oxidative damage and enhance DNA repair is emphasized. This review reveals the intricate mechanisms by which oxidative stress triggers DNA damage and its subsequent impact on neuronal health. By conducting a comprehensive literature search across various databases, we explore the molecular pathways involved, including mitochondrial dysfunction, inflammation, and altered signaling pathways, which exacerbate neuronal death and dysfunction. Furthermore, we investigate potential therapeutic strategies targeting oxidative stress and DNA repair mechanisms, focusing on antioxidant approaches, gene editing technologies, and pharmacological interventions to mitigate oxidative damage. Understanding the relationship between oxidative stress, DNA damage, and neurodegeneration is essential for developing effective therapies to slow down or stop the worsening of these disabling illnesses.