Building on its enormously successful “Whole Genome Sequencing” Project, which identified nearly 1,000 new genetic mutations in more than 50 different genes, Cure Alzheimer's Fund has announced a new, even more ambitious multiyear, $50 million plus program titled “Genes to Therapies” (G2T). Simply put, the new project’s goal is to use the most promising recent genetic discoveries to develop drugs that would stop the disease at three separate stages:
New research by David Holtzman, M.D. at the Washington University School of Medicine points to a sleep regulation protein in the brain as a possible target for Alzheimer's disease treatment or prevention. The protein, called orexin, plays a role in rousing the brain from sleep.
Recent months have witnessed three remarkable developments in projects supported by Cure Alzheimer’s Fund.
“For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease.”
A new "alternative amyloid hypothesis” from the lab of Dr. Charles Glabe, at the University of California at Irvine, helps explain precisely how neurons (nerve cells) die in Alzheimer’s disease and how known genetic mutations initiate a chain reaction in this long process. The important new hypothesis was driven by research supported by Cure Alzheimer’s Fund, and has just been being published in the Journal Neurobiology of Disease. Dr.
A promising first-in-class drug stimulates the creation of new nerve cells in the brains of Alzheimer's mice and will soon be tested in the brains of human patients, thanks to new research by Dr. Sam Gandy, member of Cure Alzheimer's Fund's Research Consortium, at Mount Sinai School of Medicine in New York.
The world already is very familiar with both Alzheimer’s disease (AD), primarily a disease that occurs in the elderly, and Down syndrome (DS), a genetic condition present at birth. What many don’t realize is that these two conditions also overlap. By age 40, nearly all people born with Down syndrome have begun accruing the plaque and tangle hallmarks of Alzheimer’s. By age 60, most exhibit signs of dementia.
Five new publications by Gal Bitan, Ph.D., and colleagues of the David Geffen School of Medicine at UCLA have been released on developing the "molecular tweezer"* CLR01 as a therapeutic drug for Alzheimer's disease and other amyloidoses (conditions involving the build-up of insoluble amyloid proteins).
A new blood test, which has the potential to accurately diagnose Alzheimer’s disease in individuals and significantly advance drug testing and research on the disease, has been developed through grant funding by Cure Alzheimer's Fund.
The test, known as Immunosignature (IS) and developed by a team led by UCLA neurologist Lucas Restrepo, uses a special method of fluorescent tagging of antibodies in the blood to recognize an identifiable binding pattern—or antibody "signature"—associated with Alzheimer's.
A stem cell model of familial Alzheimer’s disease (FAD) was successfully generated in a recent study, allowing researchers to identify 14 genes potentially implicated in the disease. One gene in particular demonstrates the important role inflammation may play in the brain of Alzheimer’s patients. The study was completed by scientists at The New York Stem Cell Foundation (NYSCF) Research Institute in collaboration with scientists at the Icahn School of Medicine at Mount Sinai (ISMMS) and funded in part by the Cure Alzheimer’s Fund (CAF).
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