Donor Appreciation: Douglas Rosenberg
Venture philanthropist Douglas Rosenberg is focused on creating “a community of hope” as he pursues efforts to raise $10 million for a project in the Dale Bredesen laboratory aimed at developing effective treatments for Alzheimer’s disease.
“I want every donor, small and large, to realize that they can make a difference with this project,” said Rosenberg. “There has been an air of pessimism regarding efforts to tackle Alzheimer’s -- this is an opportunity to change that energy and get more people involved.”
Rosenberg’s initial investment of $3.5 million through the Ellen and Douglas Rosenberg Foundation made big headlines earlier this year and highlighted the unique partnership the retired former real estate developer has formed with Buck faculty Dale Bredesen, MD.
The two met in 2007 at a Stanford Marin Club meeting. At the time Rosenberg was in the throes of caring for his father, prominent San Francisco businessman and nationally-renowned philanthropist Claude Rosenberg Jr., who succumbed to the memory-robbing disease in 2008. His stepfather died from the condition that same year. Rosenberg lost his stepmother to the disease in 2010.
At the Stanford meeting Rosenberg heard Bredesen give an overview of his research. “It was a fresh approach – Dale was looking at the root causes of Alzheimer’s way upstream from other work I was familiar with.” The two men became friends.
Bredesen, the founding CEO of the Buck Institute, focuses on Alzheimer’s as an imbalance in signaling between neurons, rather than the current dogma that Alzheimer’s is a disease of toxicity stemming predominately from damage caused by amyloid plaques that collect in the brain. The Buck faculty member believes the plaques are an effect, not a cause of the disease. His theory explains why drug trials aimed at getting rid of the plaques have failed – his research also points the way toward what he thinks could be the first effective treatments for the disease.
“We have already identified several promising compounds that restore the balance of signaling in mice,” said Bredesen, who hopes to have potential treatments in early human drug trials within two years. “I am truly grateful for Douglas’s support of our work. I have no doubt that his commitment and faith in our efforts will have positive benefits for all of those who are involved in Alzheimer’s advocacy.”