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This project will support the launching of a comprehensive effort (integrating clinical, physiological and brain biology traits) to identify in early midlife biomarkers for Alzheimer’s disease risk informed by sex differences in brain aging and memory decline. This is one of the first projects to comprehensively assess multiple predicted biomarkers for Alzheimer’s risk in middle age and relate them to brain scans, physiology, genetics, and clinical data with a specific focus on incorporating differences between men and women in Alzheimer’s development.

Alzheimer’s Disease (AD) is a complicated disease with no effective treatment yet available.  AD is currently defined by the abundance of two insoluble proteins, amyloid-b and tau, but the amount of these proteins does not accurately predict cognitive problems in people with AD.  Recent studies have found that neuropeptides, a group of secreted proteins that can be cut down into many different, shorter peptides, are widely dysregulated in AD, and might play roles in the AD disease process.  In this proposal we investigate whether neuropeptides may be used to more accurately assess AD patients, and whether supplementation with these peptides might eventually prove a new potential therapy for AD.

Note: This grant was terminated by the investigator on November 1, 2021, when she transferred to the University of Oxford for an industry position.

Peroxisome proliferator-activated receptor delta (PPARδ) is a protein that is present in the brain. It is suggested to have important functions in brain. This proposal will help us understand its exact functions in brain. I will also test whether we can target PPARδ to treat Alzheimer’s disease (AD). 

Alzheimer’s disease (AD) is a tremendous burden and there are still no therapies available. Most clinical studies have focused on the late disease stages where neuronal damage is already severe and irreversible, however, to intervene in earlier stages, it is essential to understand how Alzheimer’s disease affects brain systems early in the disease. Beyond that, we need better markers to identify individuals at an early asymptomatic stage that will likely deteriorate in the coming years as well as measures of treatment response to assess the benefit of a treatment. Our findings will thus help to ease future research on early disease stages, will make it easier for clinical trials to find the right participants and thus hopefully help to ultimately find a cure for Alzheimer’s disease.