An editorial in the December 16, 2009 issue of the Journal of the American Medical Association by Thomas J. Montine, MD, PhD, University of Washington (UW) professor of neuropathology, and Eric B. Larson, MD, MPH, executive director of Group Health Research Institute says that two new studies point to the need for a broader scientific perspective on late-life dementia.
One study, led by Robert C. Green, MD, MPH, of Boston University School of Medicine, shows that the drug tarenflurbil—which aims to suppress the accumulation of amyloid protein (plaque) in brain tissue—did not slow cognitive decline or loss of usual daily activities.
Advertisement"This is yet another example among several drug candidates" that was shown to work in mice "but failed to translate into demonstrated benefit for patients," Drs. Montine and Larson write.
Since dementia research began, scientists have narrowly focused on Alzheimer's disease and its specific characteristics, explains Dr. Larson. "But we're now starting to see that dementia is a confluence of three common disease processes—Alzheimer's disease, vascular brain injury, and Lewy body disease—any one of which can be a target for prevention or treatment in efforts to relieve the burden of late-life dementia."
The second study, led by Wolfgang Lieb, PhD, of the Framingham Heart Study, showed that higher levels of leptin—a hormone involved in fat metabolism—is linked to reduced risk of Alzheimer's disease.
"This is a surprising new association—the magnitude and strength of which is striking," says Dr. Larson. "If it's confirmed, it could lead to further research on how lifestyle and other factors like habitual exercise figure in the prevention and treatment of age-related decline and diseases such as Alzheimer's."
Dramatically increasing global life expectancy makes it "imperative for research to find solutions that prevent, delay, slow, and treat Alzheimer's disease and related dementias," write Drs. Montine and Larson. "It would be difficult to overstate the urgency of this need."