As we age, the “wiring” of the brain—called white matter—begins to wear down. This wiring is wrapped in a protective coating called myelin, which allows brain cells to communicate quickly and efficiently. When myelin is damaged, thinking slows, memory declines, and diseases like vascular dementia become more likely. The cells that make myelin, called oligodendrocytes, are extremely sensitive to stress. Low oxygen, inflammation, and poor blood flow—common problems in ageing and vascular disease—can overwhelm these cells and lead to white matter injury. Although this type of damage is one of the strongest predictors of cognitive decline, we still do not understand why oligodendrocytes break down or how to protect them. Our team previously launched an NIH-funded study to answer these questions, but an unexpected and external financial crisis forced a sudden stop in June 2025. Despite this, we had already generated hundreds of highly valuable human tissue slides, completed animal studies, optimized advanced imaging assays, and built powerful digital pathology tools. Without emergency support, this irreplaceable work risks going unfinished. This project will allow us to complete the most important analyses and unlock the scientific insights already within reach. The bridge funding will ensure that a near-complete, high-impact dataset does not get lost due to circumstances outside the scientific team’s control. By finishing this work, we aim to identify new biological “pressure points” within oligodendrocytes that can be targeted to preserve myelin, protect white matter, and ultimately reduce the burden of vascular dementia and mixed dementias.
