Summary: A multi-institutional research team has been awarded a $9 million grant to investigate how immune-cell aging affects the risk and progression of Parkinson’s disease. The project will examine immune-cell exhaustion—sometimes described as cellular “burnout”—to understand why the disease varies so widely between individuals. By mapping immune changes across patients, the team aims to identify precise biomarkers and develop personalized, oncology-style immunotherapies to intercept neurodegeneration earlier and more effectively.
Key Facts
- Immune-Cell “Burnout” Focus: The study centers on immune-cell exhaustion, a state in which age-related and chronic stresses reduce immune cells’ functional capacity, and how this state may trigger or accelerate neurodegeneration in Parkinson’s disease.
- Personalized Neurology Paradigm: Investigators plan to adapt principles from precision oncology—profiling an individual’s immune and molecular signatures—to design targeted therapies tailored to each patient’s biological baseline.
- Explaining Clinical Heterogeneity: By comparing immune profiles across many participants, the team hopes to explain why symptoms and disease speed differ so markedly from one person to another.
- Scope and Impact: Parkinson’s disease affects more than 1.1 million people in the United States and was associated with an $82 billion annual economic burden in 2024, highlighting the urgent public-health need for improved diagnostics and therapies.
- Open-Science Toolkit: The project will produce standardized, high-quality resources and datasets managed by an internal biostatistics data core to support global researchers and reduce technical barriers in drug development.
Source: Indiana University
Project Overview
A new interdisciplinary research consortium led by scientists at the Indiana University School of Medicine, together with experts from multiple universities, will study how aging-related changes in immune cells influence Parkinson’s disease risk and progression. The team will examine both idiopathic (no known cause) and familial (inherited) cases to assess whether immune-cell exhaustion contributes to disease onset or accelerates deterioration.
Malú Gámez Tansey, PhD, professor of neurology at the Indiana University School of Medicine, is the principal investigator for this initiative, which is funded by a $9 million grant. The project is part of the Collaborative Research Network (CRN), an international, multidisciplinary effort to address high-priority questions about Parkinson’s disease. The grant was awarded by Aligning Science Across Parkinson’s (ASAP) in partnership with The Michael J. Fox Foundation for Parkinson’s Research.
ASAP is expanding the CRN to create a biological blueprint of Parkinson’s disease and build a standardized toolkit of research resources. This next phase targets the disease’s heterogeneity—why clinical presentation and progression differ across individuals—and seeks to move discoveries toward precise diagnostics and new therapies. By generating shared, high-quality datasets and materials, the team aims to lower technical barriers that can slow drug discovery and translational research.
Age is the principal risk factor for Parkinson’s disease, and immune-cell exhaustion naturally increases with age. However, the specific role of immune aging in the development and progression of Parkinson’s remains underexplored. The consortium will also investigate how lifestyle and environmental factors might interact with immune aging to influence disease trajectories.
“Our objective is to translate knowledge of immune system aging into tools that identify people at higher risk for Parkinson’s disease and to design therapies that correct dysregulated immune processes in those individuals,” Dr. Tansey said. “We hope to apply a precision-medicine model similar to that used in oncology, where treatments are matched to a patient’s unique biological profile.”
The leadership team includes specialists in neurology, immunology, neuroscience and biostatistics: Rebecca Wallings, DPhil, assistant professor of neurology at Indiana University School of Medicine; Elizabeth Bradshaw, PhD, Adler Assistant Professor of Neurological Sciences and co-director of The Carol and Gene Ludwig Center for Research on Neurodegeneration at Columbia University Vagelos College of Physicians and Surgeons; Richard Smeyne, PhD, professor and chair of the Department of Neuroscience at Thomas Jefferson University and director of Jefferson Health’s Comprehensive Parkinson’s Disease and Movement Disorder Center; and Catherine Weindel, PhD, assistant professor in the Department of Microbiology and Immunology at Tulane University School of Medicine.
“Parkinson’s disease is complex enough that no single institution can answer these questions alone,” Dr. Smeyne said. “This collaboration brings together complementary expertise in immunology, neuroscience, biostatistics and clinical care to accelerate discovery and translate lab findings to patients.”
“What excites me most is the collaborative power of this project,” Dr. Weindel said. “Integrating neuroscience and immunology will provide a more complete understanding of how immune aging may contribute to Parkinson’s disease and could guide future immunotherapeutic approaches.”
Dr. Wallings’ laboratory will focus on tracking immune-cell dysfunction over time to identify early markers of disease, monitor progression, and point to immune targets for intervention. By characterizing cellular and molecular signatures of immune aging, the team aims to discover measurable indicators that predict clinical outcomes and treatment responses.
Travis S. Johnson, PhD, assistant professor of Biostatistics & Health Data Science at Indiana University School of Medicine, will serve as data manager and a collaborating principal investigator. Additional contributors from Indiana University include Andrea R. Merchak, PhD, assistant research professor of neurology, and Nicole R. Fowler, PhD, Klapper Family Scholar in Aging and Family Caregiving Research.
Key Questions Answered:
A: Immune-cell exhaustion, often described as cellular “burnout,” develops when immune cells experience prolonged stress or age-related decline, reducing their ability to control infections and regulate inflammation. Since aging is the single greatest risk factor for Parkinson’s disease, researchers hypothesize that exhausted immune cells may either fail to protect vulnerable neurons or contribute to chronic inflammation that worsens neurodegeneration.
A: Parkinson’s disease is heterogeneous: some people face rapid motor decline, others have slow progression or prominent non-motor symptoms. By studying both idiopathic and familial cases alongside environmental and lifestyle influences, the team will correlate individual immune-aging profiles with specific clinical patterns. Identifying distinct biological signatures could reveal drivers of these differences and point to tailored diagnostic and therapeutic strategies.
A: In oncology, clinicians use molecular and immune profiling to select therapies that match a patient’s tumor and immune environment. The investigators aim to apply that precision approach to neurology: by finding measurable immune markers in blood or cerebrospinal fluid, clinicians could screen aging populations, identify which biological systems are failing in an individual, and offer targeted immunotherapies to prevent or slow neurological damage.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by staff.
About this Parkinson’s disease research news
Author: Rory Appleton
Source: Indiana University
Contact: Rory Appleton – Indiana University
Image: The image is credited to Neuroscience News