Hippocampal activation is associated with longitudinal amyloid accumulation and cognitive decline

Dementia refers to the loss of intellectual or thinking abilities and Alzheimer’s disease is its most common cause. Although we don’t understand the cause of Alzheimer’s disease, we know that at early stages of the disease a protein known as beta-amyloid becomes deposited in the brain in the form of plaques. Evidence suggests that this beta-amyloid is harmful to brain cells. Although we don’t know why amyloid is deposited, research in animal models suggests that the activity of the brain cells themselves may lead to its deposition. We can measure brain activity in living people using a technique known as functional magnetic resonance imaging (fMRI), and we can also measure amyloid deposition using positron emission tomography (PET scanning). Leal et al. have now used these techniques to learn about how brain activity might influence amyloid deposition. Volunteers initially performed a memory task while their brain activity was measured using fMRI. This gave a “baseline” level of brain activity. Over the course of several years, the volunteers returned for PET scans and further memory tests. Cognitively normal older adults with greater baseline levels of brain activity – particularly in the hippocampus, a brain region involved in the formation of new memories – showed more beta-amyloid accumulation over the next three to four years. Furthermore, people who accumulated more beta-amyloid also showed a more severe decline in memory. To strengthen these results, a follow up study should be performed that examines how brain activity and amyloid deposition change together over time. In addition, it will be important to test whether methods that reduce brain activity could affect amyloid deposition, thus perhaps reducing the risk of Alzheimer’s disease.