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Cracking the Alzheimer’s Code: How Brain Trauma Triggers Disease

Niklas and Ilknur. Photo.
Experimental scientist Ilknur Özen and Niklas Marklund, professor at Lund University and neurosurgical consultant at Skåne University hospital have in collaboration with Uppsala investigated brain tissue from 15 patients. Photo: Tove Smeds

A study at Lund University reveals that traumatic brain injury alters the small vessels in the brain, resulting in an accumulation of amyloid beta — a hallmark of Alzheimer’s disease. The findings suggest that vascular dysfunction could be an early driver in neurodegenerative disorders rather than being caused by neuronal damage. The study is published in Acta Neuropathologica.

An increased risk of dementia among individuals exposed to brain trauma, traumatic brain injury, has been known for almost a century. Still, we know very little about the molecular causes behind this, which makes it difficult to find effective treatments to prevent dementia development among those affected with traumatic brain injury. But a research team at MultiPark, Lund University argues that the blood vessels in the brain holds keys to future therapies. 

Brain trauma usually impairs cerebral blood flow, possibly through pathological changes in the vascular smooth muscle cells in the vascular wall. These blood flow impairments can lead to secondary brain injuries, worsening the damage to the brain, although it remains unknown exactly how this occurs. 

To bridge this gap, Niklas Marklund, professor at Lund University and neurosurgical consultant at Skåne University hospital, decided to take a deeper look into the molecular details together with the experimental scientist Ilknur Özen. In collaboration with Uppsala University, they investigated brain tissue from 15 patients, surgically removed due to bleeding and swelling within a week following their  traumatic brain injuries. They found that the changes in the vascular smooth muscle cells coincided with increased aggregation of amyloid-beta, a protein linked to Alzheimer’s disease. 

Microsopy pictures of brain vessels with A-beta. Photos.
Researchers examined brain surface blood vessels. The artery lining appears blue, muscle cells regulating blood flow green, and red clusters show Alzheimer’s-linked amyloid beta. Photos: Ilknur Özen.

“We were surprised to see that also young patients displayed this accumulation of amyloid beta together with the vascular alterations caused by the brain trauma,” says Ilknur Özen, first author of the study. She continues: 

Our findings suggest that vascular changes may be more important for neurodegeneration than previously thought.”

Niklas Marklund adds: “This challenges the existing paradigm in neurodegeneration-related diseases by indicating that vascular dysfunction could be an early event that triggers the progression of amyloid-related diseases rather than being caused by neuronal damage.”

While aging leads to functional changes in the vasculature, brain trauma may exacerbate and accelerate these processes even in younger patients. Still, far from everybody affected by brain trauma develops Alzheimer’s disease. That is why more research is needed. 

“We are not there yet, but hopefully, increased knowledge about what is happening at a molecular level in the blood vessel cells following brain trauma opens possibilities for novel treatments,” ends Niklas Marklund. 


 

Ilknur. Photo.
Photo: Tove Smeds

Ilknur Özen

Researcher at Lund University

ilknur [dot] ozen [at] med [dot] lu [dot] se (ilknur[dot]ozen[at]med[dot]lu[dot]se) 

Profile photo of Niklas Marklund.
Photo: Mikael Wallerstedt

Niklas Marklund

Professor at Lund University

Consultant neurosurgeon at Skåne University hospital

niklas [dot] marklund [at] med [dot] lu [dot] se (niklas[dot]marklund[at]med[dot]lu[dot]se)

Link to Niklas Marklund's profile in the LU Research Portal

Twitter: @LabLubin