Summary: A multi-institutional research team has received a $9 million grant to study how aging and functional decline in immune cells influence the risk and progression of Parkinson’s disease. The project will map immune system changes associated with cellular “burnout,” seek biomarkers that explain why the disease behaves so differently across patients, and pursue precision immunotherapy strategies modeled on oncology to intercept neurodegeneration at earlier stages.
Key Facts
- Immune-cell “burnout” focus: The study centers on immune-cell exhaustion—an age-related loss of immune function—and how this breakdown may trigger or accelerate neuronal damage.
- Personalized neurology approach: Investigators plan to adapt the precision medicine model used in cancer care by profiling patients’ immune systems to guide individualized treatments.
- Explaining heterogeneity: By comparing immune signatures across many patients, the team aims to clarify why Parkinson’s onset, symptoms, and progression vary so widely.
- Public health and economic impact: Parkinson’s affects more than 1.1 million people in the U.S. and imposed an estimated $82 billion annual burden in 2024, making new therapeutic strategies a high priority.
- Open-science resources: An internal biostatistics and data core will produce standardized, high-quality datasets and tools for the global research community to lower technical barriers to drug development.
Source: Indiana University
Overview
A research consortium led by scientists at Indiana University School of Medicine, together with collaborators from several universities, will investigate how immune system aging contributes to Parkinson’s disease. The project specifically targets immune-cell exhaustion in both idiopathic (unknown cause) and familial (genetic) forms of Parkinson’s, aiming to connect changes in immune function with disease risk and clinical course.
Malú Gámez Tansey, PhD, professor of neurology at Indiana University School of Medicine, will serve as the principal investigator. The work is funded by a $9 million grant awarded to the team to join the Collaborative Research Network (CRN), an international, multidisciplinary initiative supported by Aligning Science Across Parkinson’s (ASAP) in partnership with The Michael J. Fox Foundation for Parkinson’s Research (MJFF).
ASAP’s expansion of the CRN seeks to chart a biological blueprint for Parkinson’s disease and to build a standardized toolkit of research resources. This phase emphasizes understanding disease heterogeneity—why Parkinson’s varies by individual—and accelerating the translation of discoveries into precise diagnostics and targeted therapies. Producing common, high-quality data resources is intended to reduce technical obstacles that currently slow therapeutic development.
Age is the strongest known risk factor for Parkinson’s. Immune-cell exhaustion naturally increases with age, but its direct contribution to Parkinson’s pathogenesis remains underexplored. The team will also examine whether lifestyle and environmental exposures influence immune aging and disease onset.
“Our goal is to use what we learn about immune system aging to identify people at higher risk and to target the dysregulated processes in those individuals with treatments designed specifically for them—much like the cancer field does today,” Dr. Tansey said.
The leadership team brings together experts in immunology, neuroscience, biostatistics and clinical care: Rebecca Wallings, DPhil (assistant professor of neurology, IU School of Medicine); Elizabeth Bradshaw, PhD (Adler Assistant Professor of Neurological Sciences at Columbia University); Richard Smeyne, PhD (professor and chair of Neuroscience at Thomas Jefferson University); and Catherine Weindel, PhD (assistant professor of Microbiology and Immunology at Tulane University School of Medicine).
“Parkinson’s is complex enough that no single center can answer these questions alone,” Smeyne said. “This collaboration brings complementary strengths together and helps move findings from the laboratory toward patient care more efficiently.”
Weindel emphasized the collaborative scope: “Combining expertise in neuroscience and immunology will give a fuller picture of how immune aging could contribute to Parkinson’s disease and may point toward future immunotherapy approaches.”
Wallings’ laboratory will examine how immune cells lose function over time and whether those changes correspond with early disease signs, measurable progression markers, and immune-targeted treatment opportunities.
“Parkinson’s varies widely between patients, and we lack clear explanations for those differences,” Wallings said. “By measuring immune-cell exhaustion and biological immune aging, we aim to find markers that predict progression or treatment response.”
Travis S. Johnson, PhD, assistant professor of Biostatistics & Health Data Science at IU School of Medicine, will manage the project’s data core and serve as a collaborating principal investigator. Andrea R. Merchak, PhD, and Nicole R. Fowler, PhD, will also contribute from IU.
Key Questions Answered:
A: Immune-cell exhaustion—often described as cellular “burnout”—occurs when immune cells are exposed to chronic stress or the cumulative effects of aging, reducing their ability to respond to threats or regulate inflammation. While aging is the main risk factor for Parkinson’s disease, researchers are still defining how this immune decline contributes to neuronal loss. Exhausted immune cells might fail to protect vulnerable neurons or could promote long-term inflammation that accelerates degeneration.
A: Parkinson’s is heterogeneous: some patients experience rapid motor decline, others progress slowly or present non-motor symptoms. By profiling immune aging in both idiopathic and familial cases and accounting for environmental and lifestyle factors, researchers will look for immune signatures that correlate with specific clinical patterns. Identifying these biological subtypes can explain individual differences and guide tailored interventions.
A: Modern oncology uses detailed molecular and immune profiling to match patients with therapies tailored to their tumor and immune characteristics. The team aims to bring this paradigm to neurology: discovering measurable immune markers in blood or cerebrospinal fluid could enable screening, risk stratification, and delivery of targeted immunotherapies before widespread neurological damage occurs.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The referenced journal paper was reviewed in full.
- Additional context was added by editorial 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