A scientist at the Gladstone Institutes has identified how the lack of a brain chemical known as dopamine can rewire the interaction between two groups of brain cells and lead to symptoms of Parkinson's disease. This discovery offers new hope for treating those suffering from this devastating neurodegenerative disease.
A scientist at the Gladstone Institutes has discovered a novel way to convert human skin cells into brain cells, advancing medicine and human health by offering new hope for regenerative medicine and personalized drug discovery and development.
The Gladstone Institutes today announced plans to create a Center for Comprehensive Alzheimer's Disease Research, offering new hope for the millions of families stricken by this debilitating neurodegenerative disease.
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.