UCLA researchers uncover key mechanism of brain repair in vascular dementia, revealing promising therapeutic target
Peer-Reviewed Publication
In honor of Alzheimer's Awareness Month, we’re exploring the science and stories surrounding Alzheimer’s disease.
Updates every hour. Last Updated: 22-Jul-2025 18:11 ET (22-Jul-2025 22:11 GMT/UTC)
A new study from UCLA Health has uncovered how inflammation in brain blood vessels exacerbates damage in vascular dementia and demonstrated that targeting this process with a repurposed drug can promote brain repair and functional recovery in mice.
A new study from scientists at the Buck Institute for Research on Aging has revealed a surprising player in the battle against Alzheimer’s disease and other forms of dementia: brain sugar metabolism. Published in Nature Metabolism, the research uncovers how breaking down glycogen—a stored form of glucose—in neurons may protect the brain from toxic protein buildup and degeneration. In addition to providing a new approach to Alzheimer’s research, the study could explain why GLP-1 drugs show promise against dementia
USC researchers have identified a new brain imaging benchmark that may improve how researchers classify biologically meaningful changes associated with Alzheimer’s disease, especially in Hispanic and non-Hispanic white populations. Using an advanced brain imaging scan called tau PET, the research team studied over 675 older adults from the Health and Aging Brain Study–Health Disparities (HABS-HD) aiming to identify the optimal brain signal that distinguishes individuals with clinically-relevant biological markers of AD from those who are aging normally. They compared tau PET scans of study participants who were cognitively impaired with those who were not impaired based on cognitive tests to establish a tau cut-point that would indicate a higher risk for Alzheimer’s disease. The team used a new imaging tracer called 18F-PI-2620, to measure tau protein buildup in the brain. They found that when tau levels in the medial temporal lobe—a region deep in the brain—exceeded a certain threshold, it strongly indicated cognitive impairment related to AD. But the tau cut-point was only effective when another abnormal protein, amyloid, was also present in those with cognitive impairment, and it only worked for Hispanic and non-Hispanic White participants. In non-Hispanic Black participants, the tau cut-point did not perform as expected. This suggests that other pathologies or conditions may be driving cognitive decline in this group. The findings reflect a growing focus in AD research on making sure diagnostic tools work for everyone—not just in narrow clinical trial populations.