5.4 million Americans have Alzheimer's disease (AD) costing $185 billion annually, while 15 million caregivers look after these individuals. AD is the sixth leading cause of death, but the only one in the top 10 causes that cannot be prevented.
This study may demonstrate exercise in an amount attainable by many will be preventative in asymptomatic individuals including those with brain Abeta deposition already that are at impending risk of the disease. Sperling and colleagues(1) coined the research term AD-pathophysiological process (abbreviated AD-P) for use in studies such as the intervention in this proposal.
Our long term goal is to assess whether exercise may be preventative of AD at older ages (=73, mean=75), when more than 40% of cognitively normal persons have A beta deposits, the hallmark of AD pathogenesis, in their brains. In a NIH RO1 grant submission the investigators proposed to conduct a partially blinded controlled preventative trial in 150 cognitively normal individuals, randomized in a 2:1 ratio to 18 months of moderate aerobic exercise versus 18 months of toning and stretching. All persons would have baseline and 18 month brain Abeta PET studies. The study was designed to determine whether an exercise intervention in persons mean age 75 would lead to decreased brain Abeta accumulation, increased hippocampal volume, improved cognition, and improved dementia-related biomarkers compared to the control group. The study would be unique in that the investigators would be able to examine if aerobic exercise slows the accumulation of brain Abeta in an older population, at which time Abeta deposition is common. If successful, this would provide an additional motivating reason to recommend exercise for most elderly persons.