The Gladstone Institutes has been named America's best place to work in academia, capping a seven-year stint in which readers of The Scientist have ranked the independent biomedical-research organization among academia's top ten places to work.
Scientists at the Gladstone Institutes have identified a drug candidate that diminishes the effects of both Alzheimer's disease and Huntington's disease in animal models, offering new hope for patients who currently lack any medications to halt the progression of these two debilitating illnesses.
The Hellman Family Foundation has donated $1 million to the Gladstone Institutes to help spur the development of medications for Alzheimer's disease.
A scientist at the Gladstone Institutes has made two significant stem-cell discoveries that advance medicine and human health by creating powerful new approaches for using stem cells and stem-cell-like technology.
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. Humans with Alzheimer's disease and mice genetically engineered to simulate the disease have abnormally low levels of an enzyme called EphB2 in memory centers of the brain. Improving EphB2 levels in such mice by gene therapy completely fixed their memory problems. The findings will be published in the November 28 issue of the journal Nature.
Scientists at the Gladstone Institute of Neurological Disease (GIND) have offered new information about the events that underlie the “spread” of Alzheimer's disease throughout the brain. The research, published in the November 4th issue of the journal Neuron, follows disease progression from a vulnerable brain region that is affected early in the disease to interconnected brain regions that are affected in later stages. The findings may contribute to design of therapeutic interventions, as targeting the brain region where Alzheimer's disease originates might be simpler than targeting multiple brain areas.
Alzheimer's disease is an extremely complicated disease. Several proteins seem to be involved in its cause and progression. For example, the lipid-transport protein apolipoprotein E4 (apoE4) is the major genetic risk factor for Alzheimer's disease, and apoE4 carriers account for 65–80% of all Alzheimer's cases, but exactly how apoE4 contributes to the disease is unclear.
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.
Amyloid beta (Αβ) proteins, widely thought to cause Alzheimer's disease, block the transport of vital cargoes inside brain cells. Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that reducing the level of another protein, tau, can prevent Aβ from causing such traffic jams.
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. The agreement funds research at the Gladstone Center for Translational Research led by Gladstone investigator Katerina Akassoglou, PhD, and establishes the new Lundbeck Center for Neurovascular and Immuno-imaging at the Gladstone Institute of Neurological Disease.