DNA damage in CTE Mirrors Accelerated aging, Links to Alzheimer’s, New Research Finds
BOSTON – A groundbreaking study reveals that chronic traumatic encephalopathy (CTE), a neurodegenerative disease linked to repetitive head trauma, is associated with extensive DNA damage in brain cells strikingly similar to that seen in Alzheimer’s disease and equivalent to over a century of normal aging. researchers at Boston University have identified a importent increase in “indels”-insertions or deletions of DNA base pairs-within teh neurons of individuals with CTE,suggesting inflammation triggered by head trauma drives long-term genomic instability.
The research, led by Dr.jesse Mez at BU’s School of Medicine, found thousands of these indels, potentially enough to cause “serious dysfunction or death in the affected cells,” according to Dr. Mez’s colleague, Dr. Michael walsh. While the study didn’t directly measure inflammation,prior work by Dr. Ann McKee, a neuropathologist at the BU CTE Center, and neuroscientist John cherry has demonstrated “widespread activation of microglia”-the brain’s immune cells-in CTE brains.
“We think CTE might be a combination of repeated head trauma and inflammation,” Walsh said. “That combination may bombard the genome with the same kinds of damaging processes that ultraviolet light causes in skin or tobacco smoke in the lungs,” as both UV and tobacco exposure trigger DNA damage.
The findings suggest that repeated head impacts initiate an inflammatory response, which than promotes the accumulation of DNA mutations, ultimately leading to neuron dysfunction and cell death. This points to a potential common pathway in neurodegenerative diseases. The team is now investigating whether similar inflammation-driven DNA damage occurs in other conditions like amyotrophic lateral sclerosis (ALS) and Huntington’s disease.
“This could be a common final pathway across diseases,” Walsh said.”We’d like to trace the biochemical steps from inflammation to neuron death and figure out where we can intervene.”
