Cure Alzheimer's Fund: Targeting Breakthrough Research

Henry McCance, Cure Alzheimer’s Fund co-founder and chairman emeritus, Greylock Partners, was a keynote speaker at Venture Summit East 2010. This two-day gathering highlighted the significant economic, political and technology trends impacting the global growth investor and was held at Harvard Business School. Venture Summit East features the most influential institutional investors, venture capitalists, corporate buyers, investment bankers and research analysts in the eastern United States in keynote presentations and panel debates.

Cure Alzheimer's Fund awarded the University of Texas Health Science Center and the University of Houston a $150,000 grant to fund important Alzheimer's research. The grant will give researchers the opportunity to accelerate their use of nanotechnology and new imaging techniques to study the effects of certain compounds of the Amyloid-Beta protein. Click on the link to read the article in full: http://www.

Cure Alzheimer's Fund's very own Dr. Sam Gandy is leading a team of researchers pioneering the support of oligomer research -- and they are seeing big results. According to Gandy's team of researchers, brain plaques -- long thought to be major cause of Alzheimer's -- may actually play a protective role.

  Jeff Morby, Chairman and co-founder of Cure Alzheimer’s Fund, was a featured panelist at the Milken Global Conference in Los Angeles on Wednesday, April 28. The presentation was titled, “Alzheimer’s Disease: Meeting the Challenges of an Aging Society”.  Click here to watch Jeff, Harry Johns, the President and CEO of the Alzheimer’s Association and Greg Simon, the Senior Vice President for Worldwide Policy for Pfizer, address the need for a national strategy to battle the disease.

Research consortium member, Dr. Sam Gandy, has developed a new approach for studying brain synapses that has begun to yield valuable information about the production of Amyloid-Beta oligomers, known to play a role in the onset of Alzheimer's disease. By better understanding how Abeta clumping is regulated, researchers can learn how to prevent, stop or slow Alzheimer's pathology.

Breakthrough research conducted by our very own Dr. Rudy Tanzi and his team at Massachusetts General Hospital has led to an important advancement in the understanding of the protein associated with Alzheimer’s disease. The prevailing theory has been that this protein -- A-beta -- has no function other than as a waste product created by the brain.

Testing the amyloid hypothesis of Alzheimer’s disease in vivo By Sam Gandy In this issue of The Lancet Neurology, Rinne and colleagues1 report something of a breakthrough by demonstrating the feasibility of eventually testing the so-called amyloid hypothesis of sporadic Alzheimer’s disease in vivo. According to their analysis, a passive immunotherapy protocol with an amyloid-β monoclonal antibody (bapineuzumab) was associated with a decrease in the cerebral PET signal after administration of the amyloid plaque imaging compound carbon-11-labelled Pittsburgh compound B (11C-PiB). This finding of a change in PiB signal over time is exciting, and the interpretation favoured by the authors is that the new results suggest that bapineuzumab has increased the clearance of cerebral amyloid β.

Cure Alzheimer's Fund's Dr. Rudy Tanzi was quoted in the Boston Globe in response to two new studies, one ruling out a drug called tarenflurbil and another showing an association between an appetite-controlling hormone and a lower risk of developing Alzheimer's.

Letter from the Founders: Why You Should Care About Alzheimer's Currently, for every dollar spent on Alzheimer's care, only a penny is spent working toward a cure. This is a bad equation for a disease that is estimated will cost well more than $100 billion in care (Medicare and Medicaid alone) in 2009. Cure Alzheimer's Fund focuses on research that is speed-driven, results-oriented and innovative to stop a disease that will strike half of us older than age 85.

HARRISBURG, Pa., Oct. 21 -- Governor Edward G.