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.
Scientists at the Gladstone Institute of Neurological Disease (GIND) and Stanford University have shown how key circuits in the brain control movement. The research, published in the journal Nature not only establishes the function of these circuits, but offers promise for treating movement related disorders, such as Parkinson's disease.
The Institute for Systems Biology (ISB) of Seattle, WA, is collaborating with the Gladstone Institute of Neurological Disease (GIND) and its Taube-Koret Center for Huntington's Disease Research to use whole-genome sequencing to identify genes and novel drug targets related to the onset and progression of Huntington's disease (HD). The research team, led by GIND associate director and senior investigator Steven Finkbeiner, MD, PhD, will also use induced pluripotent stem (iPS) cells from patients with HD to screen for drugs that might delay, prevent, or even reverse this devastating condition.
Lennart Mucke, MD, Director of the Gladstone Institute of Neurological Disease (GIND), has been named a recipient of the American Academy of Neurology's prestigious Potamkin Prize. Mucke is recognized for the development of experimental strategies to make the brain more resistant against Alzheimer's disease and for instigating a turnaround in the direction of research in this field. Mucke and his co-recipient Bruce Miller, MD, UCSF professor of neurology and psychiatry, will be presented with the prize for research in Pick's, Alzheimer's and related diseases on April 15.
Robert W. Mahley, MD, PhD, president of The J. David Gladstone Institutes, will receive Research!America's 2010 Builders of Science Award. The award recognizes his leadership as Gladstone's founding director and president, guiding its growth to become one of the world's foremost independent research institutions, known for its groundbreaking basic science and substantial impact on disease prevention.
Scientists at the Gladstone Institute of Neurological Disease (GIND) have identified the reason a key protein plays a major role in two neurodegenerative diseases. In the current edition of the Journal of Neuroscience, researchers in the laboratory of GIND Associate Director Steven Finkbeiner, MD, PhD have found how the protein TDP-43 may cause the neurodegeneration associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin-positive inclusion bodies (FTLDu). TDP-43, is the major component of protein aggregates in patients with these diseases. Mutations in the TDP-43 gene are also associated with familial forms of ALS and FTLDu.