Diagnosing Alzheimer’s disease is difficult—confirmation can be obtained only postmortem, by verifying at autopsy that the brain has an abundant amount of plaque made up of the sticky beta-amyloid protein. To gauge Alzheimer’s in living patients, neurologists must depend on time-consuming assessments of the brain’s degeneration—such as monitoring progressive memory loss—that often delay a conclusive judgment.
Now a new technique is poised to greatly speed diagnosis. Ongoing studies at Uppsala University in Sweden have shown that the chemical agent dubbed Pittsburgh Compound-B, or PIB, is a highly accurate marker of plaque buildup and that its abundance in the brain can predict whether patients with mild cognitive impairment will develop Alzheimer’s—and when that decline will likely start. “It has always been a puzzle,” says Chester A. Mathis, a radiologist at the University of Pittsburgh who pioneered the amyloid-imaging technique with Pittsburgh psychiatrist William E. Klunk. Even specialty clinics, Mathis says, have trouble distinguishing those patients whose memory loss is a prelude to Alzheimer’s from those who have another underlying cause, such as depression.
PIB works by binding to amyloid in sufficient amounts to appear in a positron-emission tomography (PET) scan image. Because PIB selectively binds to brain amyloid deposits but quickly clears from normal tissue, the chemical dye accurately indicates the amount of protein that is deposited in the living brain. Although other tracers can detect the presence of plaque, PIB is the first to show a strong ability to predict the onset of Alzheimer’s.
The technique could provide potential Alzheimer’s sufferers and their families with several years of advance warning, allowing them to prepare for the debilitating disease while delaying its arrival with diet and exercise. Even more promising, experts say, is the window of opportunity for drug intervention. Many potential Alzheimer’s drugs such as Alzhemed, now in its final clinical trial, target amyloid plaque. PIB is not only a powerful tool for studying the efficacy of these drugs; it is also a way to ensure that patients on the road to Alzheimer’s start getting treated early enough to minimize irreparable neuronal loss.
Now a new technique is poised to greatly speed diagnosis. Ongoing studies at Uppsala University in Sweden have shown that the chemical agent dubbed Pittsburgh Compound-B, or PIB, is a highly accurate marker of plaque buildup and that its abundance in the brain can predict whether patients with mild cognitive impairment will develop Alzheimer’s—and when that decline will likely start. “It has always been a puzzle,” says Chester A. Mathis, a radiologist at the University of Pittsburgh who pioneered the amyloid-imaging technique with Pittsburgh psychiatrist William E. Klunk. Even specialty clinics, Mathis says, have trouble distinguishing those patients whose memory loss is a prelude to Alzheimer’s from those who have another underlying cause, such as depression.
PIB works by binding to amyloid in sufficient amounts to appear in a positron-emission tomography (PET) scan image. Because PIB selectively binds to brain amyloid deposits but quickly clears from normal tissue, the chemical dye accurately indicates the amount of protein that is deposited in the living brain. Although other tracers can detect the presence of plaque, PIB is the first to show a strong ability to predict the onset of Alzheimer’s.
The technique could provide potential Alzheimer’s sufferers and their families with several years of advance warning, allowing them to prepare for the debilitating disease while delaying its arrival with diet and exercise. Even more promising, experts say, is the window of opportunity for drug intervention. Many potential Alzheimer’s drugs such as Alzhemed, now in its final clinical trial, target amyloid plaque. PIB is not only a powerful tool for studying the efficacy of these drugs; it is also a way to ensure that patients on the road to Alzheimer’s start getting treated early enough to minimize irreparable neuronal loss.
