Research in Brief
Dr. Croft, Dr. Golde, and colleagues used a method, consisting of thin sections of brain tissue from mice that were kept alive for months in cell culture dishes, to model how tau accumulates and changes in the brain. Their results showed that brain tissue containing the normal, nonpathological versions of tau do not form inclusions. The researchers were surprised to find that these tau inclusions weren’t just static clumps of protein.
In a study of more than 1,200 people, researchers show that individuals with higher levels of saturated fats in their blood are more likely to develop dementia, including Alzheimer’s disease.
BrightFocus-funded researchers discover a potential new treatment approach for Alzheimer’s - restoring the function of regulatory T cells (Tregs) to control the body’s immune response and suppress Alzheimer’s-associated brain inflammation.
Research suggests that changes to circulation and density of blood vessels in the eye may signal a risk of dementia and can be used as a screening tool for Alzheimer’s disease.
In animal experiments, scientists document that the APOE4 allele impacts cell bioenergetics in the entorhinal cortex, a critical brain region first damaged in Alzheimer’s disease (AD).
Scientists describe how the protein tau is modified over four decades as Alzheimer’s develops and progresses.
Inhibiting thyroid hormone (TH) activity helps protect against retinal degeneration in an animal model of AMD.
Researchers unravel the reasons why some patients have no response or diminished response over time to anti-VEGF [vascular endothelial growth factor) drugs used to treat age-related macular degeneration (AMD) and discover an innovative and effective combination therapy.
BrightFocus-funded projects get at the root of capillary stalling in Alzheimer’s disease, which reduces brain blood flow and increases risk for dementia. Evidence from mice suggests it’s not driven by diet and obesity alone, and a targeted treatment could help.
Early research shows one can prevent loss of brain nerve cell communication in Alzheimer’s disease by blocking ‘caspase’ from making toxic amyloid-beta from APP.
