"This is another finding of unknown significance, but it is a finding," said Dr. Gary J. Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City. "None of us know why these higher primates don't get Alzheimer's disease, but we don't know why humans get Alzheimer's disease either. . . Where it leads us, I don't know."
Since the amino acid sequence of human amyloid protein is different from that in monkey brains, scientists hypothesized that the structure might be different.
To test this theory, Rosen and her colleagues took PIB, widely used in clinical trials to diagnose Alzheimer's. PIB binds to amyloid deposits in live human brains, thus "lighting up" the plaques on positron-emission tomography (PET) scans.
They used PIB in brain tissue from nine deceased rhesus monkeys, six deceased squirrel monkeys, three deceased chimpanzees, nine deceased humans with end-stage Alzheimer's and three deceased older but healthy humans.
"We were able to show that, similar to what has been seen in mouse brains, PIB does not bind with high affinity to plaque in monkey or ape brains," Rosen said.
Another group of researchers at the Yerkes Center recently reported separately that a test involving infrared eye tracking may help pick up mild cognitive impairment in humans. The condition is sometimes a precursor to Alzheimer's.
Learn more about this condition at the Alzheimer's Association.
SOURCES: Gary J. Kennedy, M.D., director, geriatric psychiatry, Montefiore Medical Center, New York City; Rebecca Rosen, doctoral student, neuroscience program, Yerkes National Primate Research Center, Emory University, Atlanta; Neurobiology of Aging
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