Recent Advances

September 22, 2010

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.

September 9, 2010

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.

July 21, 2010

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.

July 7, 2010

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.

June 15, 2010

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.

February 18, 2010

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.

February 10, 2010

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.

January 13, 2010

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.

December 3, 2009

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? Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that two main causes of AD amyloid-beta (Aβ) peptides and apolipoprotein E4 (apoE4) impair the growth of new neurons born in adult brains. What is more, they have identified drug treatments that can normalize the development of these cells even in the presence of Aβ or apoE4. The findings are described in two separate papers published in the current issue of Cell Stem Cell.

October 13, 2009

The National Institutes of Health (NIH) has awarded a “Grand Opportunity” grant of $3.7 million to a consortium formed with the Gladstone Institute of Neurological Disease(GIND) and the Taube-Koret Center for Huntington's Disease Research to use stem cell technology to better understand Huntington's disease and to develop potential therapies. The consortium comprises a partnership of five leading Huntington's research laboratories at the University of Wisconsin, Massachusetts General Hospital, the University of California at Irvine, Johns Hopkins and the Gladstone Institutes. The consortium will use induced pluripotent stem (iPS) cell technology pioneered by Gladstone and Kyoto University's Shinya Yamanaka, MD, PhD, to develop human neurons with Huntingtonís disease characteristics. iPS technology enables stem cells to be generated from skin samples from adults and avoids the ethical issues surrounding the use of fetal stem cells.