A long-standing link between traumatic brain injury (TBI) and an increased risk of dementia, including Alzheimer’s disease, has been acknowledged for nearly a century. However, the molecular mechanisms that underlie this connection have remained unclear, complicating the search for effective treatments. A team of researchers from Lund University’s MultiPark strategic research area believes that the key to understanding this relationship may lie in the brain’s blood vessels.
Traumatic brain injury often disrupts cerebral blood flow, potentially due to pathological changes in the vascular smooth muscle cells that make up the walls of blood vessels. These disruptions can lead to secondary brain injuries, which exacerbate initial damage, though the precise process remains poorly understood.
To investigate further, Professor Niklas Marklund, a neurosurgical consultant at Skåne University Hospital and a researcher at Lund University, teamed up with experimental scientist Ilknur Özen. Their collaborative study, conducted in partnership with Uppsala University, analyzed brain tissue from 15 patients who underwent surgery within a week of sustaining traumatic brain injuries that resulted in bleeding and swelling. The team discovered that alterations in the vascular smooth muscle cells were accompanied by an increase in amyloid-beta aggregation—a protein closely associated with Alzheimer’s disease.
“We were surprised to find amyloid-beta accumulation in even young patients, alongside the vascular changes caused by brain trauma,” said Özen, the study’s first author.
She added, “These findings suggest that vascular changes may play a more significant role in neurodegeneration than previously understood.”
Professor Marklund remarked, “This challenges the current understanding of neurodegenerative diseases. It suggests that vascular dysfunction might be an early trigger for the progression of amyloid-related diseases, rather than a result of neuronal damage.”
While aging naturally brings about changes in the vasculature, brain trauma may accelerate and worsen these processes—even in younger individuals. However, not all people who experience brain trauma will develop Alzheimer’s disease, highlighting the need for further research to identify why some individuals are more vulnerable than others.
“We are not yet at a conclusive point, but gaining a deeper understanding of the molecular changes in blood vessel cells following brain trauma could pave the way for novel treatments,” concluded Professor Marklund.
The findings underscore the potential for new therapeutic approaches targeting vascular health as a way to prevent or delay dementia in those affected by traumatic brain injury.
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