October 9 -- Eli Lilly announced encouraging results yesterday involving their experimental drug Solanezumab. Solanezumab is an antibody aimed at lowering beta-amyloid levels in the brain. In trials lasting 18 months, patients with mild Alzheimer's symptoms taking Solanezumab showed significantly less cognitive decline -- 34% less -- compared with patients taking the placebo.
Cure Alzheimer’s Fund Research Consortium member and funded researcher Steven L. Wagner, Ph.D., Principle Investigator, Department of Neurosciences; School of Medicine, and William C. Mobley, M.D., Ph.D., Distinguished Professor and Chair of the Department of Neurosciences, both from the University of California, San Diego, discuss how research into the cause of Alzheimer’s disease brings hope to patients and caregivers, and the role that Cure Alzheimer’s plays in the process.
As a result of Cure Alzheimer’s Fund research, an integrated view of the causes of Alzheimer’s pathology has emerged. That view begins with a concept of what makes up a healthy brain. Abeta, we now know, performs a number of useful functions within the brain. In a healthy brain, moderate amounts of Abeta will be produced and cleared from time to time. Clearance is provided by several proteins, the most important of which are the APOE proteins (of which there are three variants).
A new study by David Holtzman of Cure Alzheimer’s Fund’s Research Consortium published by the journal “Science Translational Medicine” brings sharp new focus on the direct relationship between the accumulation of Abeta in the brain and notorious sleep problems associated with Alzheimer's disease. This NIH-funded study (also supported by Ellison Medical Foundation) was made possible by early pilot studies initiated by the Cure Alzheimer's Fund --- another great example of leveraging innovative research ideas into substantially funded, high impact projects.
After reading Barbara Kingsolver’s Animal Dreams in Honors English at Scituate High School, Lexie Fidas, 15, was given another class assignment—to create a difference in society, much the way the characters in
the book did.
A study just published in the New England Journal of Medicine points to the value of conducting a new series of Alzheimer's prevention studies, suggests Cure Alzheimer's Consortium member Sam Gandy in an accompanying NEJM editorial. The study, led by Washington University's Randall J. Bateman, found that patients with a more genetic-oriented form of Alzheimer's experience a rise in beta-amyloid (Aβ) up to 25 years before symptoms begin -- and an increased level of tau protein up to 15 years before symptoms.
On Friday, August 24, Eli Lilly announced that their beta-amyloid immunotherapy (solanezumab) failed to meet its primary clinical endpoints for Alzheimer's disease. This disappointment follows the recent failure of another promising beta-amyloid immunotherapy, bapineuzumab from Pfizer/Johnson and Johnson-Jannsen/Elan. Both drugs failed in Phase 3 clinical trials, where they were being tested for their actual effect on Alzheimer's patients.
The David K. Johnson (DKJ) Foundation was created in 2000 in honor and memory of David and Susan Johnson of Reading, Mass., to promote awareness of and provide support for individuals and families affected by Alzheimer’s disease.
A new study of an existing drug for immune disorders that may have positive effects for Alzheimer’s patients has attracted national attention lately. While phase III clinical trial results for Gammagard, an IVIG or “intravenous immunoglobulin therapy” by Baxter International are not expected until early 2013, hope for success must be balanced with a hard look at the data. The Wall Street Journal’s story on this drug and the prognosis for success by Dr.
It was announced yesterday that Bapineuzumab, the Abeta immunotherapy drug, failed to meet cognitive and functional goals in a late stage trial of Alzheimer's patients who carry the APOE4 variant. “There was no reason to believe, unless there was a miracle, that this would be positive. It will only be the results of the non-APOE4 carriers that will inform us about the future [of bapineuzumab].” said Rudolph Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School and MGH in Boston and Chair of the Cure Alzheimer’s Research Consortium.
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