BOSTON, Mass. — Stress can do terrible things to the human body. Researchers say it can even cause people to age prematurely. A new study finds stress, specifically PTSD, can also do this to the brain as well. A team from Boston University School of Medicine (BUSM) finds the condition can have a devastating interaction with one particular gene that makes a patient’s brain older than it really is.
The study by BUSM and the National Center for PTSD at VA Boston Healthcare System reveals the klotho gene is a key to longevity in humans. The new report finds a variant of this gene interacts with post-traumatic stress disorder. This leads to accelerated aging in brain tissue.
Previous studies had already uncovered this link between PTSD and biological age after measuring factors in the blood. The new report is the first to examine brain tissue and stress-induced aging.
How PTSD is linked to cellular aging
Researchers were able to gather this data by examining brains donated to the VA National PTSD Brain Bank. The team studied how the genetic variations in klotho and PTSD combined, which predicts both biological age and gene expression.
The results show older adults dealing with PTSD also suffered from accelerated epigenetic aging in their brains if they had an “at risk” form of the klotho gene. Study authors followed up with molecular experiments which reveal the changes in the normal klotho may be responsible for this aging.
Both PTSD and klotho genes have connections to inflammation, metabolic diseases, and neurodegenerative conditions like Alzheimer’s disease. PTSD is a psychiatric disorder that typically occurs after someone has experienced a traumatic event. Also known as “shell shock,” PTSD affects around 3.5 percent of U.S. adults each year, according to the American Psychiatric Association.
“This work allows us to better pinpoint who is at risk for accelerated cellular aging, and possibly, premature disease onset (such as neurodegeneration). This can help to identify the populations at greatest risk so that targeted treatments can be matched to the individuals who need it most. As well, the results point to potential therapeutic targets (klotho) in the development of pharmacological approaches to slow the pace of cellular aging,” says lead author Erika Wolf in a university release.
The study appears in the journal Neuropsychopharmacology.