The silent saboteur: oxidative stress and the path to cognitive dysfunction.

Abstract

Oxidative stress (OS) plays a central role in age-related cognitive decline and neurodegeneration and is increasingly recognized as a key factor in the pathogenesis of Alzheimer's disease (AD) and Parkinson's disease (PD). Elevated OS biomarkers are detectable from the earliest stages of these disorders. In this critical narrative review, we explore the bioenergetic cascade underlying neurodegeneration, emphasizing pathophysiological alterations, mechanisms, and therapeutic targets. Recent evidence suggests that OS and impaired cellular energy dynamics are both early markers and downstream effects of neuroinflammation, contributing to symptom severity and reduced treatment efficacy. A deeper understanding of these interrelated processes is essential for the development of more effective interventions. Monitoring OS-related metabolites may offer a promising strategy for identifying therapeutic targets and enabling early clinical intervention, ultimately aiming to reduce neuroinflammation and improve patient outcomes in AD and PD.