Unraveling the Triggers to Myelin Damage in Alzheimer’s Disease

The project aims to uncover how vascular dysfunction and blood proteins drive myelin damage in Alzheimer’s disease and explore treatments that can restore brain repair and improve cognitive function.

Myelin damage has emerged as a key player in Alzheimer’s disease (AD). However, the triggers of myelin pathology in AD remain largely unknown. Fibrinogen, a blood clotting protein deposited in the AD brain, is a potent inducer of neurotoxic inflammation and inhibitor of myelin repair. We will determine the role of fibrinogen on myelin-forming cells in AD mice with state-of-the-art imaging, multiomic technologies, and behavioral analysis of learning and memory in AD mice, as well as testing pharmacologic treatments promoting remyelination.

What’s most unique and innovative about this project is its focus on myelin, an often-understudied aspect of Alzheimer’s disease, and how blood proteins and vascular dysfunction drive its damage and impair brain repair. The project uses cutting-edge imaging, multiomic profiling, and, importantly, tests innovative remyelinating therapies aimed at restoring brain repair and enhancing cognitive functions. This integrated, cross-disciplinary approach aims to uncover breakthrough strategies to restore myelin, promote brain repair, and improve memory and learning in Alzheimer’s.

Once this study is complete, it could open the door to new therapeutic interventions that promote brain repair and improve cognitive function in people with Alzheimer’s disease. By uncovering how vascular dysfunction and blood proteins drive myelin damage, the research may shift the field’s focus toward targeting brain repair mechanisms. Ultimately, these advances could lead to innovative therapies that improve the quality of life for patients and families affected by Alzheimer’s.