Understanding the relationship between sleep, the amyloid beta diurnal pattern, and Alzheimer’s disease
Alzheimer’s disease is the most common cause of dementia in the United States and a growing public health problem. Pathologically, Alzheimer’s disease is characterized by the extracellular deposition of amyloid-β (Aβ) in the brain and intracellular tangles of tau. Deposition of Aβ in the brain appears to be a key first step in the pathogenesis of Alzheimer’s disease. Recent work at Washington University has shown that Aβ fluctuates with the sleep-wake cycle (i.e. a diurnal pattern), although the relationship of this oscillation to the development of Alzheimer’s disease is unknown. My research program is focused on understanding the relationships between sleep, the Aβ diurnal pattern, and Alzheimer’s disease. My research occurs in both in the laboratory and at the Washington University Multidisciplinary Sleep Medicine Center. I am involved with several on-going studies. My research group is studying if changes in sleep affect Aβ concentration and kinetics (i.e. production and clearance) in humans using stable-isotope labeled peptides. I am also an investigator on the Healthy Aging and Senile Dementia program project grant through the Knight Alzheimer Disease Research Center where we are monitoring sleep-wake activity in older adults to correlate with changes in cognitive function, CSF biomarkers, brain MRI, and amyloid imaging. Through these studies, we hope to establish if sleep may be used as a potential diagnostic, theranostic, or preventive treatment for Alzheimer’s disease.