Scientists at The Ohio State University Wexner Medical Center have gotten the evidence that traumatic brain injuries (TBI) could heighten the risk of developing Alzheimer’s disease. This study had involved both animal models and human brain tissue. It sheds light on how TBIs may trigger harmful protein build-ups in the brain, leading to cognitive issues associated with Alzheimer’s. A key aspect of the research points to a protein called BAG3, which plays a critical role in removing harmful proteins from the brain. Enhancing this protein could potentially reduce the risk of Alzheimer’s in individuals who have experienced TBI.

How TBIs May Lead to Alzheimer’s Disease

Each year, about 2.5 million individuals suffer from TBIs, with many facing an elevated risk of Alzheimer’s later in life. The research team, led by Dr Hongjun “Harry” Fu, Assistant Professor of Neuroscience, sought to uncover the molecular mechanisms connecting TBI to Alzheimer’s. By examining mouse models and human post-mortem brain samples, they found that TBIs increased the presence of hyperphosphorylated tau proteins—known for their role in Alzheimer’s disease. These proteins, along with other factors like synaptic dysfunction, create the ideal conditions for cognitive decline.

The Potential Role of BAG3 Protein in Prevention

Researchers has noted that the downregulation of BAG3 after TBI contributes to the accumulation of tau proteins in neurons. By using a gene therapy approach to increase BAG3 levels, they were able to reverse some of the damage, improving brain function and clearing out harmful proteins. This suggests that targeting BAG3 might be a viable strategy for preventing Alzheimer’s disease following brain injury.

Next Steps in Research

As part of ongoing research, scientists are using a model known as CHIMERA, which closely mimics the effects of mild TBIs in humans. This will help further explore how TBI and Alzheimer’s are connected, offering potential new treatments for reducing Alzheimer’s risk post-TBI.