Research in Briefs
BrightFocus-funded researchers—assisted by a citizen science video game-- were among the first to show that Alzheimer’s contributes to stalls in the brain’s tiniest blood vessels, and they’re working on possible treatments.
Scientists have discovered that a rare version of the so-called “neutral” APOE3 genotype, one they’ve named APOE3-Jacksonville (APOE3-Jac), may help protect against Alzheimer’s through its effects on brain metabolism.
Years ago, a BrightFocus grantee said it might be possible to manipulate the blood-brain-barrier to treat Alzheimer’s disease. Now his hypothesis is driving an international effort to develop drugs for this purpose.
New evidence shows the same molecular pathway contributes to inflammation in AMD and lupus, helping to drive a hyperactive immune response in both diseases. The discovery could fast-track development and approval of existing anti inflammatory drugs to treat AMD.
Why does the impact of an Alzheimer’s risk factor vary by race and genetic ancestry? Researchers are learning the answers.
BrightFocus-funded researchers were among the first to “map” the normal 3D structure of a protein called myocilin, which is abundant in the drainage pathway of the eye. Now, with a second grant, they’ve designed antibodies to help diagnose and treat myocilin misfolding as it contributes to glaucoma.
Early research suggests that modifying cross-talk between the eye’s immune and vascular systems may be a new way to treat AMD.
Extracellular vesicles isolated from the blood of people with Down syndrome-related Alzheimer’s disease have been shown to seed toxic tau species in the brains of normal mice, shedding light on the uptake and transmission of toxic tau.
As retinal cells transition from one state to another, they exhibit molecular changes that correspond to those of liver cells.
Tau tangles tend to accumulate in brain cells that also express the Wolframin-1 protein—a discovery that’s been corroborated in human tissue and a mouse model.
