Reactive oxygen species (ROS) contribute to oxidative stress, which plays a critical role in aging and neurodegenerative diseases such as Alzheimer’s disease and dementia. Among ROS, hydrogen peroxide is known to particularly target lipids and impair neuronal function. Although the body possesses antioxidant defense mechanisms, their efficiency declines with age.

In this study, we investigated the effects of low concentrations of hydrogen peroxide on cultured neuronal cells. Treatment induced neurite degeneration characterized by bead-like swellings [1]. This degeneration was associated with disrupted calcium homeostasis and a marked increase in mitochondrial superoxide production [2]. Electron microscopy revealed abnormal accumulation of mitochondria at the beaded regions of neurites [3].

These findings suggest that ROS-induced neurite degeneration occurs prior to neuronal cell death and involves mitochondrial dysfunction driven by calcium dysregulation. Such early pathological changes may increase our understanding of neurodegenerative disorders. Antioxidant supplementation could represent a potential strategy to mitigate oxidative neuronal damage during aging.