News Release: Research

Apr. 1,  2009

Yerkes Researchers Closer to Determining Why Humans Develop Alzheimer's Disease

Finding Could Shed Light on Why Only Humans Develop Neurodegenerative Diseases and Pave the Way for New Treatment Approaches

From Woodruff Health Sciences Center

Researchers at the Yerkes National Primate Center, Emory University, have discovered a compound used to diagnose Alzheimer’s disease in humans may also be useful in determining why humans develop the disease and other primates do not.

The study, available in the current online issue of Neurobiology of Aging, has moved the scientific community another step closer to understanding why age-related neurodegenerative diseases, such as Alzheimer’s disease, are uniquely human and is providing new insights into potential therapeutic targets for these disorders.

The study focused on Pittsburgh Compound B (PIB), a radiolabeled compound used to diagnose Alzheimer’s disease in humans by positron emission tomography (PET). When injected into the bloodstream, PIB enters the brain and binds to the beta-amyloid plaques that are thought to be a key feature of Alzheimer’s disease. 

The brains of nonhuman primates generate beta-amyloid protein that has the same amino acid sequence as that in humans.  Furthermore, monkeys and great apes develop abundant beta-amyloid plaques as they age. Nonhuman primates, however, do not become demented, nor do they have some of the other brain lesions typical of Alzheimer’s disease. To determine if there is a structural difference in the beta-amyloid proteins humans and nonhuman primates produce, the researchers used PIB to analyze post-mortem brain tissue from aged rhesus macaques, squirrel monkeys, chimpanzees, humans with end-stage Alzheimer’s disease and humans with aged but healthy brains.

Lead researchers Rebecca Rosen, a doctoral student who is conducting her research at Yerkes, and Lary Walker, PhD, a neuroscientist and research professor at Yerkes, in collaboration with Harry LeVine III, PhD, at the University of Kentucky, found PIB did not bind to beta-amyloid proteins in the brains of the nonhuman primates, even if the brain contained more beta-amyloid protein than a human counterpart. This finding indicates “PIB may be useful in determining why humans develop Alzheimer’s disease and other primates do not,” explains Walker.

As many as five million Americans are living with Alzheimer’s disease, the most common form of dementia.

“A cure has eluded researchers, and the disease is progressive and fatal,” states Rosen. “That’s why it’s so important we narrow in on the huge number of potential causes of Alzheimer’s disease. By studying the development of human features of the disease that occur naturally in nonhuman primates, we may be able to isolate what makes people so susceptible to neurodegenerative disease and identify targets for therapeutics.”


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