One of the daunting aspects of Alzheimer’s disease is that it is seldom diagnosed until victims have already lost significant cognitive function. Even if treatments are developed, they will not have sweeping impact unless early-detection methods are devised. One step toward this grail may come from psychiatrist and brain researcher Eric Reiman of the Banner Alzheimer’s Institute in Phoenix. He has been using positron-emission tomography (PET) to study cognitively healthy people at three levels of genetic risk for the disease—those with two copies, one copy or no copies of the apolipoprotein E type 4 (APOE4) gene, which has been implicated in autopsies of Alzheimer’s victims. Reiman says that APOE4 carriers show reduced metabolism in brain regions known to be affected by Alzheimer’s disease and that “these reductions become more pronounced over time.” He and his colleagues plan to use PET to evaluate high-risk groups as various therapies are undertaken, to try to reveal if a therapy shows any effect. “Our goal is to find an effective way to prevent [Alzheimer’s] without having to lose a generation along the way,” Reiman says. Scott Small, a neurologist at Columbia University, is using magnetic resonance imaging to define an early-warning clue in the hippocampus, vital to memory. “By imaging Alzheimer’s patients over time,” he explains, “we have found which parts of the hippocampus have neuronal dysfunction.” The pattern of dysfunction in Alzheimer’s is different from that in normal aging. “We could use this knowledge both to diagnose [Alzheimer’s] in its earliest stages,” Small says, “and to test new drugs to see if they arrest cell loss in these special regions.”
One step toward this grail may come from psychiatrist and brain researcher Eric Reiman of the Banner Alzheimer’s Institute in Phoenix. He has been using positron-emission tomography (PET) to study cognitively healthy people at three levels of genetic risk for the disease—those with two copies, one copy or no copies of the apolipoprotein E type 4 (APOE4) gene, which has been implicated in autopsies of Alzheimer’s victims. Reiman says that APOE4 carriers show reduced metabolism in brain regions known to be affected by Alzheimer’s disease and that “these reductions become more pronounced over time.” He and his colleagues plan to use PET to evaluate high-risk groups as various therapies are undertaken, to try to reveal if a therapy shows any effect. “Our goal is to find an effective way to prevent [Alzheimer’s] without having to lose a generation along the way,” Reiman says.
Scott Small, a neurologist at Columbia University, is using magnetic resonance imaging to define an early-warning clue in the hippocampus, vital to memory. “By imaging Alzheimer’s patients over time,” he explains, “we have found which parts of the hippocampus have neuronal dysfunction.” The pattern of dysfunction in Alzheimer’s is different from that in normal aging. “We could use this knowledge both to diagnose [Alzheimer’s] in its earliest stages,” Small says, “and to test new drugs to see if they arrest cell loss in these special regions.”
