Call for Proposals: 2026 Pilot Projects for ME/CFS Research [Deadline Extended]

The Cornell Center for Enervating NeuroImmune Disease invites applications for pilot funding to advance ME/CFS research. Eligible PIs must hold appointments on the Cornell Ithaca campus (including graduate students, postdoctoral researchers, and research associates, as well as others who meet Cornell’s PI eligibility requirements); co-investigators from Weill Cornell Medicine are welcome. Proposals (as a single PDF) are due by 5 PM ET on October 1 October 8, 2026, and should be emailed to the Center’s manager, Carl Franconi, at carl.franconi@cornell.edu. A complete description of the program, including formatting, award amounts, and reporting requirements, can be found on the Pilot Projects page.

Watch Now: Dr. Maureen Hanson on the Biology of Post-Exertional Malaise

A talk from Dr. Maureen Hanson, Center Director, is now available on YouTube as part of Action for ME’s PRIME webinar series. In her presentation, “Molecular Signals of PEM,” Dr. Hanson shares findings from recent Center studies analyzing blood samples collected from ME/CFS patients and sedentary healthy controls before and after two consecutive maximal cardiopulmonary exercise tests. This research offers insight into the biological mechanisms underlying post-exertional malaise (PEM)—a hallmark and defining symptom of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Watch the talk on YouTube (starting at 2:12:40) to learn more about these important findings.

Center Investigators Attend Invest in ME Research 2026 Conference Week; Early Career Researcher Wins Outstanding Presentation Award

Center investigators recently participated in the Invest in ME Research 2026 conference week at the Wellcome Genome Campus in Cambridge, UK, attending both the 15th Biomedical Research into ME Colloquium (BRMEC15) and the 18th International ME Conference. This annual gathering represents one of the most significant forums for ME/CFS research collaboration, bringing together international researchers, clinicians, and patient advocates to advance understanding of myalgic encephalomyelitis. Our Center’s continued participation reflects our commitment to fostering global partnerships and contributing to the growing body of biomedical research addressing this complex disease.

Erin Wissink, PhD

We’re particularly proud that one of our early career investigators, Dr. Erin Wissink, received 1st place for the Outstanding Oral Presentation Award from Young EMERG for her talk entitled “Cytotoxic T cell dysregulation in ME/CFS.” The presentation outlined a hypothesis that metabolic differences in T cells in ME/CFS cause changes in mTOR signaling and mRNA translation, based on findings from our recent single-cell genomics dataset. This recognition highlights the innovative research emerging from our Center and the importance of supporting early career scientists in ME/CFS research, particularly as the field continues to expand with growing recognition of post-viral illness connections.

Center Director Maureen Hanson Visits WE&ME Foundation

Our Center Director, Dr. Maureen Hanson, recently visited the WE&ME Foundation in Vienna, Austria, in her role as a member of their Scientific Advisory Board. During her visit, the Foundation announced a new research funding initiative on June 15, 2026. This collaboration reinforces our Center’s commitment to advancing rigorous, patient-centered ME/CFS research and strengthens our partnerships within the global research community.

The WE&ME Foundation’s call for proposals seeks research teams focused on advancing understanding of the biological mechanisms of ME/CFS. Projects must demonstrate innovation in methodology or clinical approach and include meaningful involvement of patients or patient representatives, with study designs aligned with current diagnostic criteria. The initiative welcomes applications from both established ME/CFS researchers and scientists from related fields, encouraging diverse approaches to the field. Research teams investigating post-viral contexts are also eligible, provided participants meet established ME/CFS diagnostic criteria.

We encourage members of the research community to explore this funding opportunity and share it with colleagues who may be interested. Learn more on the WE&ME Foundation Call for Proposals for full eligibility details and deadlines.

Uncovering Protein Signatures of Post-Exertional Malaise in ME/CFS

Graphical abstract by Arnaud Germain, Ph.D.

Post-exertional malaise (PEM) is the hallmark symptom of ME/CFS: an exacerbation of symptoms triggered by physical or mental exertion that is often disproportionate to the activity. While PEM has long been recognized as central to ME/CFS, the molecular mechanisms underlying this debilitating response have remained largely unknown.

A recent paper from the Center, published in Molecular & Cellular Proteomics, provides a comprehensive look at what happens at the protein level when people with ME/CFS experience PEM. The work was led by first author and Center investigator Arnaud Germain, a postdoctoral research associate in the Hanson Lab. The paper has also been featured in an article on Medscape.

What Was Done

The study used a powerful aptamer-based proteomic assay (the SomaScan 7K) to measure 6,361 unique plasma proteins in 132 individuals (79 ME/CFS cases, 53 age/BMI-matched sedentary controls). The design included two maximal cardiopulmonary exercise tests (CPET) separated by 24 h, enabling the investigators to chart the molecular aftermath of exertion and recovery.

By comparing ME/CFS to sedentary controls rather than healthy active individuals, the team could distinguish disease-specific alterations from changes simply due to physical  deconditioning, a key approach that differentiates this study from others.

Key Findings

Our analysis revealed widespread proteomic changes following exertion, with the most dramatic alterations occurring in ME/CFS participants during the 24-hour recovery period—precisely when PEM symptoms typically emerge.

Immune System Dysfunction:

  • Suppression of T and B cell signaling
  • Reduced IL17 and cell-cell communication pathways

Metabolic Disruption:

  • Up-regulation of glycolysis/gluconeogenesis pathways, consistent with mitochondrial stress and impaired immune recovery
  • Disrupted associations between protein levels and physiological performance (VO₂max, ventilatory anaerobic threshold) in ME/CFS compared to controls

Clinical Correlations:

  • Correlations between immune-related proteins and symptom severity, including muscle pain, recurrent sore throat, and lymph node tenderness

Sex Differences:

  • Sex-stratified analyses revealed distinct molecular responses in females and males, emphasizing the critical importance of considering sex as a biological variable in future research

Key Insights

For Patients: This research provides molecular validation for what ME/CFS patients have long known—that their bodies respond abnormally to exertion. The recovery phase in ME/CFS is characterized by prolonged, maladaptive molecular responses rather than a healthy return to baseline. This data provides scientific backing for clinical recommendations around pacing and avoiding activities that trigger PEM.

 For Researchers: The findings reveal that immune, metabolic, and neuromuscular pathways remain dysregulated in ME/CFS long after exertion ends. The study also demonstrates that women and men with ME/CFS may exhibit different molecular pathophysiology, emphasizing the need to account for sex differences in future studies.

 For the Field: This work provides a rich molecular dataset and a foundation for mechanistic follow-up. The longitudinal dynamic profiling approach may also serve as a model for investigating other disorders featuring exertion intolerance (e.g., Long COVID).

Access the Research

The full manuscript is now available in Molecular & Cellular Proteomics:

Germain A, Glass KA, Eckert MA, Giloteaux L, Hanson MR. Temporal dynamics of the plasma proteomic landscape reveals maladaptation in ME/CFS following exertion. Molecular & Cellular Proteomics (2025). doi: https://doi.org/10.1016/j.mcpro.2025.101467

The associated dataset can be accessed on the journal’s website and on mapMECFS.

Center Graduate Student Researcher Wins Award at International Conference

Anne Gardella, a graduate student researcher in the Cornell Center for Enervating NeuroImmune Disease, has been awarded the Research Insight prize at the 2025 ME Research UK Virtual Poster Competition hosted by IACFS/ME. Gardella’s winning poster focused on cell-free RNA research in ME/CFS at the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis’s virtual conference held October 22-25, 2025. This recognition highlights the cutting-edge ME/CFS research being conducted at Cornell and demonstrates the Center’s commitment to advancing our understanding of ME/CFS through innovative biomarker discovery and molecular research approaches.

Interested in viewing the poster? Click here to see the poster in full detail.

Cell-free RNA may help us understand and diagnose ME/CFS

Great work by Center member and lead author Anne Gardella (doctoral student, De Vlaminck Lab) on demonstrating how cell-free RNA (cfRNA) in blood could help us understand—and possibly diagnose—ME/CFS. This Center-led project highlights our cross-lab collaboration, with cfRNA expertise from the De Vlaminck Lab, guidance and materials from our Center’s Administrative Core, and immune profiling resources from our Center’s Grimson Lab.

What the study did:

Our team analyzed cfRNA from plasma samples from 93 people with ME/CFS and 75 sedentary healthy controls, drawn from our Center’s prior cardiopulmonary exercise testing (CPET) study.

What the study found:

Using a machine-learning approach, the study uncovered 21 cfRNA signals that, together, identified ME/CFS cases versus controls with 0.81 AUC and 77% accuracy in a held-out test set. This is promising research, but not yet a clinical test.

By using an immune cell “atlas” from our Center’s Grimson Lab, the team estimated where the cfRNA signals likely came from. They found differences in the relative contributions of several cell types, including plasmacytoid dendritic cells, monocytes, naive CD8 T cells, MAIT cells, and platelets.

Gene-level analyses in ME/CFS point to broad changes in immune function, extracellular matrix organization, and mitochondrial function, consistent with prior studies.

When looking at circulating viral signals, the study did not find a significant difference in overall viral burden between groups.

Why this matters:

This work advances our understanding of the biology of ME/CFS and supports the search for blood-based biomarkers. It is part of our NIH-funded U54 research program.

What’s next:

We are now studying cfRNA before and after CPET to better understand post-exertional malaise, and we are exploring how cfRNA patterns may relate to muscle and cellular function. Stay tuned for updates.

Want to read more?

The Cornell Chronicle has published a press release about this study. The full paper appears in PNAS. The Chronicle article provides background, explains the approach, and highlights key findings.

New Study Explores Autoantibody Profiles in ME/CFS Using Advanced Screening Technologies

Researchers from the Cornell Center for Enervating Neuroimmune Disease, Fred Hutchinson Cancer Center, Yale School of Medicine, and Augmenta Bioworks have published a study investigating autoantibody patterns in ME/CFS. The research, published in the International Journal of Molecular Sciences, represents an in-depth look at the involvement of autoimmunity in ME/CFS.

The study examined blood samples from a substantial cohort of 172 participants who were evaluated at multiple sites across the US. All ME/CFS patients met the Canadian Consensus Criteria for diagnosis and developed their condition prior to 2020, ensuring their illness was not related to the COVID-19 pandemic.

Using two sophisticated platforms – a 1,134 autoantibody Luminex panel and Rapid Extracellular Antigen Profiling (REAP) – researchers examined over 7,500 antibody-antigen interactions. Unlike previous studies, this comprehensive analysis found no significant differences in autoantibody reactivities between ME/CFS patients and controls. This includes previously reported targets such as β-adrenergic receptors and other G protein-coupled receptors. The results indicate that the role of autoantibodies in ME/CFS needs further investigation.

The paper is available through open access, and we encourage those interested to read the full publication for more detailed information.

Graphical abstract by Arnaud Germain, Ph.D.

New Research Links T Cell Exhaustion to ME/CFS

A new study from our Center, recently published in the Proceedings of the National Academy of Sciences (PNAS), has revealed important insights into how ME/CFS affects the immune system. The research team, led by Associate Director Andrew Grimson, discovered that patients with ME/CFS show signs of T cell exhaustion, a condition where immune cells become less effective at fighting infections. This finding helps to better understand the chronic nature of the disease and may open new paths for treatment approaches.

Fig. 5 Model of proposed ME T cell mechanism of action via exhaustion.
Source: PNAS publication

The Cornell Chronicle has published an accompanying article about this research, offering a detailed look at the study’s implications for ME/CFS patients. The article explains how the research team conducted their investigation and what these findings might mean for future treatment strategies. You can read the full Cornell Chronicle coverage to learn more about this significant development in ME/CFS research.

Recruitment information for muscle and cellular function study

We are seeking volunteers comprising 40 ME/CFS patients and 20 controls to participate in an NIH funded (U54AI178855) project. An overview of the study can be found here. Only those participants whose onset of ME/CFS was before 2020 will be eligible. Please review our recruitment flyer for more information on how to volunteer as a patient or control in this research study.

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