My goal as a researcher is to understand the pathophysiology of Alzheimer’s disease (AD). No one measure provides a thorough characterization of the AD disease trajectory. Instead, a multidimensional approach is needed to integrate intersecting measures of biology and cognition. In my work I regularly study healthy aging and AD using magnetic resonance imaging (MRI), positron emission tomography (PET), cognitive testing, and biofluid assays. In my research studying late-onset AD I have examined the role that apolipoprotein polymorphisms have on longitudinal atrophy and beta-amyloid accumulation, I’ve examined how both cerebrospinal fluid and neuroimaging markers predict longitudinal cognition, and I’ve related changes in functional MRI to AD biomarkers. My work with autosomal dominant Alzheimer’s disease (ADAD) similarly has taken a multimodal approach. 

I’ve examined how baseline levels of beta-amyloid PET predict longitudinal cognitive change, how neuroimaging biomarkers emerge and spread spatially in the brain, and the temporal time course of longitudinal change in CSF, neuroimaging, and cognitive measures. The common theme across my work has been to examine multiple biomarkers in parallel to gain a richer understanding of the pathobiology of the disease. My work serves to bridge multiple disciplines together to better understand AD. My ongoing work will continue this theme. In particular, working with Dr. Anne Fagan, I’m interested in how novel fluid (YLK-40, SNAP-25, NFL) markers of neural injury relate to other AD biomarkers and cognition. These markers are particularly noteworthy, as they are relatively low cost and can serve as innovative biomarkers in both clinical and research settings.

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