Aging is a natural process characterized by a gradual decline in physiological functions, which increases vulnerability to diseases and mortality.

This decline is influenced by oxidative stress and inflammation, with epigenetic mechanisms playing a critical role in regulating metabolism and energy expenditure.

The oxidative stress theory connects aging-related changes to reactive oxygen species (ROS) and reactive nitrogen species (RNS), which contribute to the development of diseases prevalent in older populations.

As individuals age, they face an increased risk of various diseases, including cardiovascular diseases, cancer, and neurodegenerative disorders.

Neurodegenerative diseases, such as Alzheimer's, exhibit a doubling risk for onset approximately every five years, underscoring the link between aging and cognitive impairments.

Research indicates that ferroptosis, a form of programmed cell death characterized by iron-dependent cell death, may be involved in neurodegenerative disorders, contributing to cognitive decline.

Despite being less studied than other mechanisms like apoptosis, ferroptosis presents significant implications for understanding cell death in aging.

During ferroptosis, notable changes occur in mitochondria, including alterations in membrane structure and overall mitochondrial shape.

Iron plays a crucial role in cellular processes, necessitating precise regulatory control over its levels in the body to prevent detrimental effects.

Erastin has been identified as a ferroptosis inducer, showing potential therapeutic implications due to its selective cytotoxicity against certain cancer cell types.

Future research on ferroptosis could reveal new therapeutic targets to mitigate neurodegenerative diseases, leading to improved treatment strategies.

The free radical theory of aging, proposed in the 1950s, suggests that reactive oxygen species generated from mitochondrial respiration cause cumulative damage to essential macromolecules.