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Cell type-specific peripheral immune response as a biomarker and therapeutic target for Alzheimer's disease

Award Number: F32AG094162
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/04/2027
PERIOD OF PERFORMANCE END DATE: 03/03/2028

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Cell type-specific peripheral immune response as a biomarker and therapeutic target for Alzheimer's disease - PROJECT SUMMARY Alzheimer’s disease (AD) affects over 55 million people worldwide. AD therapies have met with limited success and clinical trials are pointing to earlier intervention as critical for success. Prediction of disease risk is difficult and currently relies on the detection of biomarkers present only after disease symptoms or neurodegeneration begins. There is a crucial need for biomarkers capable of predicting disease long before it starts. Recent studies revealed that individuals with certain autoimmune disorders are at a significantly higher risk for AD than the general population, but that systemic immunosuppressant treatment brings these individuals’ AD risk below that of the general population. These observations suggest that immune dysfunction contributes to AD. If so, the immune system might be a good source of early markers of AD. Given the easy access to blood for diagnostic purposes, I propose to look for biomarkers of AD in blood cells. We have previously identified an AD-specific phospho-protein signature within the peripheral (blood) immune cells of AD patients dependent on immune response to stimulants that mimic inflammation, infection, or autoimmune reactions. The predictive power of this signature is limited, because we only sampled a small number of phosphoproteins. Here, I will use single-cell RNA sequencing and machine learning to compare immune responses to stimulation in peripheral blood samples from AD and healthy control donors and identify the differences with the greatest diagnostic potential (Aim 1). Then, I will determine if our AD-specific phosphoprotein signature can be used to predict AD early by screening the peripheral blood of patients who presented healthy at the time of blood draw but who were later diagnosed with AD (Aim 2). Altogether, my work will determine the diagnostic potential of peripheral immune cell activity for AD. The Corces Lab at Gladstone Institutes and the Montine Lab at Stanford University are the ideal places both for this research and my development into an independent investigator. Dr. Ryan Corces is a world leader in single-cell genomics analysis with extensive expertise in large-scale omics analysis both for neurological and immunological diseases. Dr. Thomas Montine is a leader in neuro-immunology and pathology for neurodegenerative diseases and a pioneer of research into the effect of Alzheimer’s on the peripheral immune system. Their co-mentorship, combined with the highly supportive and enriching environments of Gladstone Institutes, Stanford, and UCSF, and my own experience in immunology, memory neuroscience, assay development, and bioinformatic analysis, will help me carry out this project successfully and acquire the professional skills I need to launch on my path to independence.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $79,348 )
2026	2026	J.DAVID GLADSTONE INSTITUTES	1650 OWENS ST	SAN FRANCISCO	CA	94158	SAN FRANCISCO	USA	Aging Research	000	1	9/4/2026	NEW	$79,348
														Subtotal = $79,348

Grand Total All Awards = $79,348

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Cell type-specific peripheral immune response as a biomarker and therapeutic target for Alzheimer's disease

Award Number: F32AG094162

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/04/2027

PERIOD OF PERFORMANCE END DATE: 03/03/2028

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