Reisa Sperling, MD, a Harvard-based, BrightFocus-funded Alzheimer’s researcher now leading a major clinical trial, thinks it might be possible to prevent or delay the worst symptoms of Alzheimer's when physical changes in the brain, including shrinkage and amyloid build-up, are detected early, before cognition is impaired, and treatment begins at those earliest stages.
Thanks to the mammoth worldwide effort to collect genetic information on glaucoma patients, there’s been a major breakthrough with the discovery of several new gene variants associated with severe glaucoma. The latest discoveries double the number of genes found through earlier studies and lend hope that genetic screening can be used to identify and direct treatment for people at highest risk of losing their sight.
There’s been a major discovery from Washington University in St. Louis (WUSTL). In mice studies, researchers have shown that fibroblast growth factor (FGF) proteins, a family of “signaling proteins” involved in tissue formation, can be independently manipulated to bring about desired results in individual organs without disrupting the organism as a whole.
Recently, the BrightFocus Foundation awarded an Alzheimer’s Disease Research Fellowship to Soong Ho Kim, PhD, at Mount Sinai Hospital in New York City, to study whether a new drug could directly attack symptoms of Alzheimer's disease, but also work to address the disease process. A new study in Molecular Psychiatry now provides evidence that this line of research may be progressing."
Now that the entire human genome, or set of genes, has been mapped and is at our disposal, the promise of gene therapy lies with being able to “edit” genes as they vary from individual to individual in ways that either cause or might be used to prevent a disease. Recently, a Johns Hopkins research team headed by BrightFocus Grantee Don Zack, MD, PhD, announced they’ve improved upon the state-of-the-art tool for manipulating the genome in research settings.
Researchers from Yale School of Medicine have discovered a promising new drug compound that reverses some Alzheimer’s effects on memory in mice. They found that a protein drug compound, known as TC-2153, blocks the Alzheimer’s disease linked effects of another protein called striatal-enriched tyrosine phosphatase (STEP). At high levels, STEP prevents synaptic strengthening in the brain—something vital to memory function.
The week of July 20-24, 2014 brought the International Society for Eye Research (ISER) biennial meeting to U.S. shores. In San Francisco, ISER 2014 drew 800 scientists from 37 countries to hear about the latest in vision research.
Recent BrightFocus grantees, Vinit B. Mahajan, MD, PhD, and co-investigator Jessica M. Skeie, PhD, of the University of Iowa mapped the location and quantities of some 4,403 different proteins expressed in the retinal pigment epithelium (RPE) and choroid of the healthy human eye.
This molecular map now provides clues as to why certain areas of the choroid are more sensitive to certain diseases, as well as where to target therapies and why.