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Aiming to End Alzheimer Disease

Aiming to End Alzheimer Disease
Rudolph E. Tanzi, left, with USC Davis School's Caleb Finch.

The USC Davis School of Gerontology welcomed Potamkin Prize winner Rudolph E. Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School, on April 9 to discuss how genes affect Alzheimer disease.

“There is some level of genetic involvement in every case of the disease,” he said, offering a special acknowledgement to the seminal work of USC professor Margaret Gatz, who in 2006 revealed a genetic cause in up to 80 percent of Alzheimer cases.

Taking Gatz’s research a step further, Tanzi asserted, “Even sporadic cases, such as head trauma and stroke that bring on Alzheimer disease, still have a genetic component.”

Such assertions have made Tanzi an international and controversial figure in Alzheimer disease research. His goal is to help “eradicate” the disease by 2020.

“The way to do this in the future is by never letting it strike,” he said, outlining three essential components necessary to achieve this aim.

First, early prediction would require the identification of the entire set of genes affecting Alzheimer disease. Second, early detection would allow for the use of biomarkers, such as measuring protein levels of spinal fluid, to help identify individuals who are at-risk.

Third, early prevention would allow for lifestyle changes such as physical fitness, healthy diet and available drugs to treat those individuals predisposed to the disease.

To make it all happen, Tanzi called for $5 billion per year in federal funds. This figure represents an exponential increase from the roughly $640 million in federal funding spent last year on Alzheimer disease research. In fact, under the previous presidential administration, he said, appropriations for Alzheimer disease research declined.

“When I made this proposition at a White House conference last week, nobody even batted an eye,” he said. “The cost of the disease is predicted to ruin the current Medicare and Medicaid systems if there is no change. Already, the disease sucks up nearly one-third of costs.”

The projected annual price tag for treating Alzheimer disease by 2030 – $470 billion – drew a smattering of groans from the audience of about 125 faculty members, students and friends of the USC Davis School, who peppered him with questions throughout the discussion.

Tanzi, by now, is unfazed by crowds of any kind. Growing up, he played rock keyboards, including gigs with Steve Winwood and Chuck Mangione. He even considered a career in music, but gave it up after being struck in the head by a guitar during a concert.

Instead, he went on to be part of the research team that found the Huntington disease gene in 1980. Seven years later, he co-discovered the first Alzheimer gene APP (amyloid beta precursor protein), while researching Down syndrome. Tanzi has since been involved with co-discovering two more of the four known Alzheimer disease genes, called “presenilins,” which are mutations that account for up to half of early-onset familial Alzheimer disease.

He predicts that there could be “dozens” or even “hundreds” of other genes with various effects on the disease. Those four recognized genes, he said, only account for 30 percent of the genetic causes for the disease.

“There is still 70 percent of the genetic puzzle that we don’t know,” he added.

In 2008, Tanzi co-wrote a paper classifying four new Alzheimer genes, and as a result was ranked fifth in Time magazine’s “Top Ten Medical Breakthroughs of 2008.”

“Every new gene gives you a new window into the disease, a new idea about the cause, and a new idea for a novel therapy or drug for treating the disease,” he said.

Tanzi also emphasized the importance of the Alzheimer Research Forum, a database that aims to provide a comprehensive, unbiased and regularly updated collection of genetic association studies performed on Alzheimer’s disease phenotypes. On its Web site,, publications are identified following systematic searches of scientific literature databases, as well as the table of contents of journals in genetics, neurology and psychiatry.

He also gave a great deal of credit to the work of the USC Davis School’s Caleb Finch, a University Professor.

“His research is 10 years ahead of everyone else’s,” Tanzi said.

Tanzi concluded by offering new evidence that the neurotoxic amyloid peptide implicated in Alzheimer disease may be a result of immune responses to common infections. His research has revealed powerful antibiotic activities, which, he believes, evolved as an ancient immune defense molecule.

Finch called this discovery “revolutionary.”

“In earlier times, when lifespans were shorter, the amyloid response could have been beneficial, but slowly developing consequences on the brain only became recently important with our longer lifespans,” he said.

Gatz, who was also in attendance, was impressed as well. “What Professor Tanzi does is lay out the whole story of the biology of Alzheimer disease, from the genes to the symptoms, in a way that illuminates the next step of scientific research necessary to prevent this disease and perhaps achieve the goal of a world free of dementia,” she said.

Dean Gerald C. Davison called the discussion “a wonderful conclusion to our six-part Andrus Gerontology Center/AARP Distinguished Lecture Series.”

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