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New Insights into Cause and Prevention of Alzehimer's Disease
Leading researcher to speak at University of Utah, call for alternative models of disease causation
Sep 3, 2009 10:00 AM
SALT LAKE CITY – Over 500,000 scientific papers have been published on the amyloid plaque theory for the causation of Alzheimer’s Disease, with no explanation for the production or function of the amyloid beta peptide, which occurs in normal cells, according to Dale Bredesen, MD, Principle Investigator and Founding CEO of the Buck Institute for Age Research. Bredesen will share his findings in two presentations at the University of Utah on September 8 and 9.
Bredesen will present his findings in a public lecture on Tuesday, September 8 at 6:00 PM at the Utah Museum of Fine Arts Auditorium. He will give a scientific lecture on Wednesday, September 9 at 9:00 AM at the University of Utah’s Clinical Neurosciences Center. Both lectures are made possible through the generous support of the Jerome Joseph Landa Memorial Lecture in the Department of Neurology at the University of Utah School of Medicine.
“Since there is still not truly effective therapy for Alzheimer’s, it is critical that alternative models be explored, and their tenets and implications confirmed or refuted,” said Bredesen. “Furthermore, research in this area may ultimately lead to new insights into other neurodegenerative diseases, such as Parkinson’s and amyotrophic lateral sclerosis (Lou Gherig’s Disease).”
In July, Bredesen was awarded a highly competitive $1.6 million dollar EUREKA grant from the National Institutes of Health to further his lab’s innovative research in Alzheimer’s Disease. EUREKA stands for Exceptional, Unconventional Research Enabling Knowledge Acceleration. The awards go to scientists proposing innovative, even controversial research that could provide a paradigm shift in dealing with a difficult biomedical problem. An estimated 5.2 million Americans have Alzheimer's, with those numbers expected to soar as the population ages. There is no effective treatment for the neurodegenerative disease.
Research in the Bredesen lab focuses on Alzheimer's as a brain signaling disorder that impacts brain plasticity, rather than the current dogma that Alzheimer's is a disease of toxicity stemming from damage caused by sticky amyloid plaques that collect in the brain.
"We are very excited to receive this award,” said Bredesen. "It points us in a new direction in Alzheimer's research, which is essential if we are to find an effective treatment for this devastating disease."
Initial studies in the Bredesen lab support the theory that Alzheimer's is a nerve signaling disorder. Research in the Bredesen lab focuses on netrin-1, a naturally occurring protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. Netrin-1 interacts with the amyloid precursor protein (APP), which is concentrated at the points where neurons connect. Even though the sticky amyloid plaques, which have been, viewed as a hallmark sign of Alzheimer's result from APP, Bredesen says it seems unlikely that APP exists simply to cause the disease. In previous studies, Bredesen and colleagues showed that APP binds to netrin-1. When netrin-1 was given to mice that have a gene for Alzheimer’s their symptoms were reversed, and the sticky amyloid was reduced.
One surprising implication of this new theory is that Alzheimer's is a "prionic" disease -- a distant, yet not necessarily contagious, cousin to Mad Cow Disease. Prions are proteins that occur normally in a harmless form. When the protein folds into an aberrant shape, the normal prion turns into a rogue agent. It then co-opts other normal prions to become rogue prions as well. Bredesen says studies are now underway to determine if netrin-1 is an anti-prion.
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Clinical Neurosciences Center Public Affairs
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