2025 New Investigator Award Winners
The National Alzheimer’s Coordinating Center (NACC) and the Alzheimer’s Association are pleased to announce the 2025 New Investigator Award winners. This newly expanded program is dedicated to mentoring and funding early career investigators focused on advancing Alzheimer’s disease and related dementias discovery and translation.
This year, 10 awardees from across the National Institute of Aging’s (NIA) Alzheimer’s Disease Research Centers program will receive $135,000 in direct costs to support their proposed projects focused on tackling a range of pressing challenges in the field.
NACC is funded by NIA and serves as the centralized data repository and collaboration and communication hub for NIA’s Alzheimer’s Disease Research Centers (ADRC) program, which encompasses 36 centers across the United States. The Alzheimer’s Association is the world’s largest non-profit funder of Alzheimer’s and all dementia science, with over $360 million in funding committed today to over 1,000 projects in 53 countries.
This year, 10 researchers were chosen from an applicant pool of 138 eligible proposals across 34 Centers. The winners also represent 10 unique Centers and institutions across the United States.
Through a partnership with the Research Education Component (REC), applicants could also participate in a mentorship program to aid them with their applications. Eighty-two percent of applicants participated in the program and were matched with a mentor. Seventy percent of the 10 awardees participated in the mentorship program and 93 percent of mentees reported that this mentorship would also be valuable for future grant applications. Mentee satisfaction rose in 2025, with 83% reporting that mentorship strengthened their proposals (up from 80% in 2024).
The 2025 winners are:
Joshua Cahan, MD
Northwestern ADRC
SAMBA: Study of Anti-amyloid Monoclonal Antibody Biospecimens and ARIA
The SAMBA: Study of Anti-Amyloid Monoclonal antibodies and Biospecimens in ARIA aims to uncover the immune alterations in amyloid-related imaging abnormalities and its possible relationship to occult cerebral amyloid angiopathy. By using transcriptomics methods, we will look at gene expression in immune cells on brain tissue and biofluids in patients receiving anti-amyloid therapy and comparing to individuals with cerebral amyloid angiopathy or cerebral amyloid angiopathy related inflammation.
Quinton Cotton, PhD
University of Pittsburgh ADRC
Advancing Intergenerational Networks for Dementia Care in Black Communities
Social connection—a sense of belonging and support—improves well-being, recovery, and quality of life. Cotton will explore how Black youth, adults, and older adults build intergenerational bonds and what strengthens them. Meaningful social connections may protect against memory loss and Alzheimer’s. This study aims to create a culturally grounded program that strengthens social ties, reduces isolation, and lowers the risk of Alzheimer’s and related dementias (ADRD) in Black communities.
Hilaree Frazier, PhD
University of Kentucky ADRC
Role of p38 MAPK in Mediating AD-Associated Myelin and Synaptic Changes
Myelin sheaths are an important component of nerve cells and are required for them to function properly. Loss of myelin is one of the first changes to occur in the Alzheimer’s disease (AD) brain, and this subsequently worsens cognitive decline and AD pathology. Using AD model mice, Dr. Frazier and colleagues will test if suppressing brain inflammation can reduce myelin deterioration and slow AD progression. The team will also evaluate myelin loss in AD patients across varying disease stages using clinical samples from the UK-ADRC.
Valentina Garbarino, PhD
South Texas ADRC
Transcriptomic Signature for Chronic Stress Contribution to ADRD Risk
Experiencing chronic stress may increase the risk of developing Alzheimer’s disease by 2-fold. However, clinical practice lacks a reliable biomarker for the evaluation of psychological stress, limiting the ability to effectively assess stress-driven Alzheimer’s disease risk, that may be targeted as an interventional strategy. The Garbarino lab will evaluate the utility of a transcriptomic blood profile associated with chronic stress, termed the Conserved Transcriptional Response to Adversity, to serve as a minimally invasive, sensitive, and modifiable with intervention, biomarker to assess psychological stress levels that may be indicative of increased neurodegenerative disease risk.
Marios Georgiadis, PhD
Stanford ADRC
Linking Myelin Pathology to Lipid Dysregulation and Disease Hallmarks in AD
Myelin, the lipid-rich multi-lamellar structure that ensheaths neuronal axons, has recently emerged as an important co-pathology in AD, possibly linked to the disease hallmarks and the known widespread lipid dysregulation reported already by Alois Alzheimer. In this project, we will use the latest tools to quantify myelin degeneration and lipid dysregulation in AD hippocampi and link them to AD proteinopathies. This will test mechanistic hypotheses of myelin involvement in AD pathogenesis and potentially provide new diagnostic and therapeutic targets.
Chad Murchison, PhD
University of Alabama at Birmingham ADRC
Areal and Individual Influences of SDOH and Disparity on ADRD and Cognition
An important class of modifiable risk factors for Alzheimer's disease are social determinants of health, with a notable subset being social disparities, differences in health outcomes linked to social, economic, and environmental disadvantages often arising from systematic inequalities. Although regional measures of disparity are widely used, they are built using different components and represent distinct facets of inequality. This research will comprehensively evaluate the associations between ADRD outcomes, several areal metrics of inequality, and the individual disparity components for those metrics using sophisticated statistical and machine learning methods.
Monica Santisteban, PhD
Vanderbilt ADRC
Unveiling the Impact of Increased Cerebrospinal Fluid Renin in ADRD
Hypertension is an important risk factor for Alzheimer's disease. We will study how the renin angiotensin system, an important molecular pathway involved in hypertension, contributes to Alzheimer's disease. Utilizing a combination of human biospecimens and mouse models, our mechanistic approach will determine the impact of cerebrospinal fluid renin activity on cognitive decline and biomarkers of AD pathology.
Nicole Scott-Hewitt, PhD
Duke/UNC ADRC
Investigating RNA-Dependent Neuroimmune Interactions in Alzheimer's Disease
Mounting genetic, molecular, and clinical evidence implicates altered neuroimmune crosstalk in Alzheimer's Disease (AD) pathology. Our proposed studies aim to investigate how early protein changes in AD impact RNA-dependent neuroimmune interactions inside of neurons, and whether these contribute to cellular and cognitive dysfunction. Understanding how these converging pathways underlie the neuropathology of AD could prove critical in interpreting patient outcomes and drug efficacy or eventually aid in the development of new therapies targeting these interactions.
Matthew Welhaf, PhD
Washington University ADRC
Pinpointing Cognitive Change in Preclinical AD Using Computational Models
In preclinical Alzheimer's disease, cognitive change is often subtle, but newer, more flexible, statistical approaches can be used to better detect changes earlier prior to symptoms onset. This has led Welhaf to ask if combining the impressive nature of the NACC dataset with these newer techniques can help stage cognitive decline (both globally and by domain) in those at risk for developing Alzheimer's disease.
Tingxiang Yan, PhD
Mayo Clinic ADRC
Defining the Role of UFMylation in Tau Secretion in Alzheimer's Disease
In Alzheimer's disease, toxic tau proteins accumulate and spread between brain cells, contributing to memory loss and cognitive decline. Yan's project investigates how an understudied protein system called UFM1 may trigger and accelerate this process by modifying tau. Uncovering how UFM1 drives tau pathology could reveal new targets to slow or prevent disease progression.