Genetic Engineering

Introduce or modify genes to fix mutations that cause age-related diseases (e.g., cancer, Alzheimer's). For example, using CRISPR to correct mutations in genes like BRCA1/2 (linked to breast cancer) or APOE4 (linked to Alzheimer's).

Upregulate genes that protect and repair cells from damage (e.g., oxidative stress, radiation). For example, boosting expression of genes like FOXO3 and SIRT1, which are associated with longevity and improved cellular repair mechanisms.

Telomeres shorten with age, leading to cellular aging. Genetic engineering could increase telomerase activity to extend telomeres.
Note: Unregulated telomerase expression is linked to cancer, so this needs careful targeting.

Reset the “epigenetic clock” by reprogramming somatic cells toward a more youthful state using genes like Oct4, Sox2, Klf4, and c-Myc (Yamanaka factors). The goal is to reverse age-related changes at the cellular level without causing tumors or loss of cell identity.

Genetically engineer immune cells (like CAR-T) or pathways to identify and clear out senescent (zombie) cells, which drive inflammation and tissue damage. Reduces chronic inflammation and improves tissue function.

Modify genes to create a more youthful or robust immune response, reducing infection risk and cancer incidence in aging populations. For example, gene editing to improve T cell receptor diversity or NK cell function.

Alter genes to improve mitochondrial efficiency, reduce reactive oxygen species, and increase metabolic health. Genes like PGC-1α, UCPs, and SIRT3 have been explored for boosting mitochondrial health.

Genetically mimic the effects of caloric restriction (CR), which is known to extend lifespan in multiple species. Genes involved: SIRT1, AMPK, and mTOR pathways—CR influences all of these.