Dr. Dale Bredesen is internationally recognized as an expert in the mechanisms of neurodegenerative diseases such as Alzheimer’s disease. He graduated from Caltech, then earned his MD from Duke University Medical Center in Durham, NC. He served as Chief Resident in Neurology at the University of California, San Francisco (UCSF) before joining Nobel laureate Stanley Prusiner’s laboratory at UCSF as an NIH Postdoctoral Fellow. He held faculty positions at UCSF, UCLA and the University of California, San Diego. Dr. Bredesen directed the Program on Aging at the Burnham Institute before coming to the Buck Institute in 1998 as its founding President and CEO.  Dr Bredesen has mentored many, many physicians and PhD learners in his lab, presented over 300 papers, written over 200 peer reviewed papers written numerous book chapters and abstracts,, written several books including his recent the End of Alzheimer’s: The first program to prevent and reverse cognitive decline, received numerous patents and honors. In addition, recently he has been interviewed on many television  and radio shows including Dr Oz. 

The uniform failure of recent drug trials in Alzheimer’s disease has highlighted the critical need for a more accurate understanding of the fundamental nature of Alzheimer’s disease. Dr. Bredesen’s research has led to new insight that explains the erosion of memory seen in Alzheimer’s disease, and has opened the door to a new therapeutic approach. He has found evidence that Alzheimer’s disease stems from an imbalance in nerve cell signaling: in the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory breaking, allowing irrelevant information to be forgotten. But in Alzheimer’s disease, the balance of these opposing signals is disturbed, nerve connections are suppressed, and memories are lost. This model is contrary to popular dogma that Alzheimer’s is a disease of toxicity, caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain — promoting signals that allow some of the nerve connections to lapse. Thus the increase in the peptide that occurs in Alzheimer’s disease shifts the memory-making vs. memory-breaking balance in favor of memory loss. This work has led to the identification of several new therapeutic candidates that are currently in pre-clinical trials.

Dr. Bredesen’s novel insights into the fundamental nature of Alzheimer’s disease recently attracted an investment of $3.5 million toward a $10 million goal for initial clinical trials of these new therapeutics. This generous support came from the private venture capitalist Douglas Rosenberg, who is helping to fund the Alzheimer’s Drug Discovery Network, centered at the Buck Institute. The unit is screening drug candidates to find those that can preserve a healthy balance in the signaling pathways that support memory. Dr. Bredesen’s work on nerve cell signaling is also the focus of a collaboration between the Buck Institute and BioMarin Pharmaceuticals, Inc., which is seeking treatments for a rare form of Alzheimer’s disease, early onset Familial Alzheimer’s Disease (eFAD), which may develop in people as young as 30 years of age.