Among over 500 tested proteins, 14 were found to have significant associations with longevity, indicating a high probability of their relationship with lifespan extension.

The study highlighted epigenetic clocks, such as PhenoAge and GrimAge, which supported the finding that increased expression of the protein PDAP1 accelerates aging processes.

Specifically, high levels of PDAP1 were associated with a nearly one-year reduction in lifespan for individuals over 60, based on data from the UK Biobank.

Experimental results demonstrated that PDAP1 is linked to cellular senescence, with its expression increasing in senescent cells and promoting faster aging in lung fibroblasts.

Silencing PDAP1 in cellular models delayed senescence, suggesting that downregulating this protein could enhance cellular longevity and improve metabolic health.

Although the study relied on genetic data and cellular models without animal testing, PDAP1 is proposed as a promising target for future drug development aimed at extending lifespan.

The research also uncovered key genetic pathways influencing common causes of death, linking specific genes to conditions such as lung cancer, stroke, and metabolic disorders.

By integrating data from various -omics sources and employing advanced statistical techniques, the researchers identified several proteins associated with lifespan extension and mortality.

A recent study published in the journal Aging Cell has established a causal relationship between multiple genes and overall mortality risk, presenting new avenues for longevity research.

The researchers utilized large genetic databases to explore connections between specific genes and longevity, particularly focusing on molecular quantitative trait loci (QTLs) to understand their influence on lifespan.

Analyzing data from over a million individuals, the research identified strong genetic correlations with lifespan, including metrics like parental lifespan and extreme longevity.