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Alzheimer’s Disease Maintaining a Healthy Brain Easier than Repairing a Damaged Brain STORY HIGHLIGHTS Patients at risk for Alzheimer’s disease should be advised of the importance of lifestyle in preventing or delaying memory impairment. Newer types of PET scans are focusing on the protein deposits that build up in the brain of Alzheimer’s patients as a potential early indicator. For the majority of patients, nongenetic factors, including lifestyle choices, are more important to their brain health. As researchers continue to move toward earlier detection of Alzheimer’s disease through improved neuroimaging strategies and genetic discoveries, a UCLA Alzheimer’s and longevity expert stresses that patients should be advised of the importance of lifestyle in preventing or delaying memory impairment — even if they have yet to show any symptoms. Although there is no cure for Alzheimer’s, finding ways to detect it at an earlier stage has significant clinical implications, says Gary Small, MD, professor of psychiatry and biobehavioral sciences in the Jane and Terry Semel Institute for Neuroscience and Human Behavior at UCLA and director of the UCLA Longevity Center. “If we can identify problems early, we have a better chance of protecting the brain while there are still intact brain cells,” Dr. Small explains. “It is easier to maintain a healthy brain than to repair a damaged brain.” Through neuroimaging and genetic studies, researchers are looking for biological markers that will help to detect Alzheimer’s before major damage has occurred. Structural imaging with MRI or CT techniques is routinely used to evaluate patients experiencing memory loss — typically to rule out possible factors such as a tumor or stroke. More revealing in early Alzheimer’s diagnosis is functional imaging with PET scans — in particular fluorodeoxyglucose (FDG) PET, which measures glucose metabolism in areas of the brain that are involved in memory, learning and problem solving. Now, newer types of PET scans are focusing on the protein deposits that build up in the brain of Alzheimer’s patients as a potential early indicator. This includes an approach developed by Dr. Small and colleagues at UCLA. “We use chemical markers that temporarily attach themselves to the abnormal protein deposits that define the disease: amyloid and tau,” Dr. Small explains. Other approaches attach only to amyloid, he notes, and tau appears to correlate more closely with the disease. Dr. Small’s group is currently studying the approach in research protocols. What is known about genetic factors falls into two categories. In rare cases, families have an autosomal-dominant inheritance pattern, meaning that half of the family members will get Alzheimer’s disease — typically with early onset. Individuals with such a family history should consult a genetic counselor and potentially be tested for the mutation that is causing the inherited form of the disease, Dr. Small says. Much more common are genetic indicators that have been found to increase the risk of Alzheimer’s. The best-understood of these is the apolipoprotein E (ApoE) gene, which has three forms: 2, 3 and 4. In the general population, it is estimated that as many as one-in-five people have ApoE4, putting them at a higher risk for Alzheimer’s disease. Because the gene is neither necessary nor sufficient to cause Alzheimer’s, Dr. Small notes, it isn’t recommended as a screening tool. It is, however, useful in research. “If we find that people with mild memory loss who have ApoE4 respond better to a treatment, that is important to know,” he says. UCLAHEALTH.ORG 1-800-UCLA-888 (1-800-825-2888)