Study finds link between head injuries and Alzheimer’s risk

Mild head injuries may raise Alzheimer’s risk later in life, but swift treatment after trauma could reduce the risk of Alzheimer’s and other long-term brain damage, new research suggests.

Lab studies found a single mild traumatic brain injury can damage the brain’s lymphatic drainage system, the waste-clearing network that removes harmful proteins.

In mice, repairing this drainage within 24 hours prevented the build-up of tau, a toxic protein linked to Alzheimer’s disease.

The research team at the University of Virginia, led by John Lukens, used an emptied virus shell to deliver a natural repair protein to the brain’s protective layers, helping damaged vessels regrow and work properly.

Lukens said: “By boosting the brain drainage using this growth factor that kind of fixes the pipes above the head that does the draining, that can provide a therapeutic treatment option to eliminate the risk of Alzheimer’s and CTE after brain injury.”

He added that there may be a crucial treatment window shortly after head trauma when long-term damage could be reduced, particularly for patients who require hospital care.

“One of the critical new experiments we’re going to have to do is see how far out the therapeutic window is, where it would still have a beneficial effect,” Lukens said.

“Obviously it would be great if we had a larger window, but at least with this, we know that targeting those who’ve had severe brain injuries that require transport and treatment at a hospital would be the ideal population to benefit at the moment.”

UVA researcher Jonathan Kipnis first identified a direct connection between lymphatic vessels and the brain in 2015.

These vessels are now known to support brain health and immune regulation; when they fail, debris clearance drops and neurodegeneration accelerates.

Lukens said the work could be especially relevant for veterans, as blast injuries often affect the meninges, where these vessels sit.

Restoring drainage may also help people at high genetic risk of Alzheimer’s and could be combined with antibody drugs that target amyloid beta.

Human trials are still years away, and Lukens said the approach is unlikely to reverse Alzheimer’s once neurons are lost. But early intervention could help prevent or slow disease progression.