SAN FRANCISCO, CA—April 26, 2012—Scientists at the Gladstone Institutes have unraveled a process by which depletion of a specific protein in the brain contributes to the memory problems associated with Alzheimer's disease.
SAN FRANCISCO, CA—Scientists at the Gladstone Institutes have discovered a key protein that regulates insulin resistance—the diminished ability of cells to respond to the action of insulin and which sets the stage for the development of the most common form of diabetes.
SAN FRANCISCO, CA—Scientists at the Gladstone Institutes, an independent and nonprofit biomedical-research organization, have identified a protein that exacerbates symptoms of Parkinson's disease—a discovery that could one day lead to new treatments for people who suffer from this devastating neu
SAN FRANCISCO, CA—Scientists at the Gladstone Institute of Neurological Disease (GIND) in San Francisco have discovered a new strategy to prevent memory deficits in a mouse model of Alzheimer's disease.
SAN FRANCISCO, CA—Alzheimer's disease is an extremely complicated disease. Several proteins seem to be involved in its cause and progression.
SAN FRANCISCO, CA—Scientists at the Gladstone Institute of Neurological Disease (GIND) have uncovered new approaches to reduce toxic proteins in Alzheimer's disease (AD) and other neurodegenerative diseases. The results might lead to new treatments for these diseases.
SAN FRANCISCO, CA—Amyloid beta (Αβ) proteins, widely thought to cause Alzheimer's disease, block the transport of vital cargoes inside brain cells.
SAN FRANCISCO, CA—The Gladstone Institutes and the international pharmaceutical company H. Lundbeck A/S have announced a collaborative research agreement to study and identify therapeutic candidates for neurological diseases.
SAN FRANCISCO, CA—Scientists at the Gladstone Institute of Neurological Disease (GIND) and Stanford University have shown how key circuits in the brain control movement.
SAN FRANCISCO, CA—Stimulating the growth of new neurons to replace those lost in Alzheimer's disease (AD) is an intriguing therapeutic possibility. But will the factors that cause AD allow the new neurons to thrive and function normally?