Written by Ashley Koca

Akin to the gene’s namesake greek goddess, Clotho, the Klotho (KL) gene is one which controls the process of senescence. The KL gene codes for longevity and based upon genotype, can increase cellular aging and the effects of neurodegenerative disorders. PTSD was the focused neurological condition in this study, but this does not discredit the likelihood of this gene’s connection to other conditions, as it is unlikely that the results are unique to PTSD. In whole, this research is the first comprehensive analysis of the connection between cellular aging and increased psychological stress through the KL gene. To investigate this connection, researchers utilized KL variants from 309 non hispanic, white veterans who have engaged in a study analyzing war-influenced neural stressors previously. Researchers collected blood to analyze DNA methylation age (DNAm), telomere length, and C-reactive protein (CRP) while also taking MRI scans to understand white matter neural integrity. Telomere length, DNAm, and CRP “inflammaging” is being used to show cellular senescence in addition to white matter integrity. displaying the impact of neurodegenerative diseases. Major findings of the study included KL types rs9315202 and rs9563121 possessing correlations to PTSD symptom severity and sleep difficulty, projecting advanced epigenetic age as well. ariant rs9315202 showed the most PTSD interaction, projecting 2 tracts worth of white matter integrity, and displaying CRP prediction. This particular SNP showed a strong connection with the extremity of metabolic syndrome—a conglomerate of different medical conditions like high blood sugar and abnormal triglyceride levels. Throughout each test, most findings were shown to be of more prevalence in older adults. This conducted research suggests potential benefits in the realm of medicine. More specifically, the study’s results implicate that the usage of klotho protein could have medicinal benefits in assisting with neurodegenerative therapy. The introduction of klotho protein fragments have been seen to improve cognitive ability in mice, the KL isoform’s increased expression within the hippocampus and prefrontal cortex improved memory, mobility, and cognitive performance, and after demyelination, overexpression was seen to cause remyelination of the corpus callosum. The downfall of this study, though, was the limitation to the majorly white male population that was used. With a more inclusive study, perhaps, a properly conclusive answer can be achieved. Regardless, this research provides hope for the future of combatting cellular aging and providing therapy for those ailed.