ME/CFS BRAC
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome Biospecimen Review Access Committee
The Myalgic Encephalomyelitis / Chronic Fatigue Syndrome Biospecimen Review Access Committee (ME/CFS BRAC) reviews applications for samples from studies of ME/CFS.
| Date Submitted | Reviewed by |
|---|---|
| October 17, 2025 - December 21, 2025 | January 21, 2026 |
| December 22, 2026 - February 12, 2026 | March 18, 2026 |
| February 13, 2026 - April 16, 2026 | May 20, 2026 |
| April 17, 2026 - June 11, 2026 | July 15, 2026 |
| June 12, 2026 - August 13, 2026 | September 16, 2026 |
| August 14, 2026 - October 15, 2026 | November 18, 2026 |
| October 16, 2026 - December 17, 2026 | January 20, 2027 |
The BRAC committee will assess the applications based on experimental rationale, feasibility/reproducibility of the assays, expertise of the investigator, availability of the institutional resources to support the study, and the statistical analysis of the number of samples required for the hypothesis testing. Investigators will be notified by email the outcome of the review (i.e. approve, approve upon revisions, or deny) within a week after the review meeting. Summary statements are released 2-3 weeks after review. For applications that were ‘approved upon revisions’, investigators will be notified about concerns that would need to be addressed before the application could move forward. Please note that the ME/CFS BRAC does not provide funding.
If sample access is approved by the ME/CFS BRAC, the two possible outcomes are:
- If the study has funding, the samples are distributed to the investigator following a virtual meeting to introduce the sample distribution process (“on-boarding”) and after fulfilment by the investigator of additional requirements specified by BioSEND (i.e. MTA, Data Use Agreement, data analysis and sharing plan). For questions, please contact Rebecca Price, Ph.D.
- If the investigator has yet to obtain funding for the study, the BRAC will issue a letter to the applicant documenting provisional access to the samples requested. This letter can be used to support an application for funding opportunities from the NIH or other organizations. Conditional approvals will be valid for a period of up to 12 months.
To facilitate scientific rigor and reproducibility, samples for approved applications are shipped blinded (each aliquot is labeled with a Sample ID). The BioSEND team will work with investigators during the onboarding call to create box designs to facilitate blinded analyses. Investigators must return their assay analyses into an appropriate data repository prior to being unblinded by BioSEND.
Assistant Professor of Medicine
Columbia University Medical Center
New York, NY 10032
Chen, Yang, DrPH
Epidemiologist
Centers for Disease Control and Prevention
Atlanta, GA 30333
Franconi, Carl, MS
Manager
Center for Enervating Neuroimmune Disease, Cornell University
Ithaca, NY 14850
Grimson, Andrew, PhD
Professor, Molecular Biology and Genetics
Cornell University
Ithaca, NY 14850
Hsiao, H Timothy, PhD
Chief Scientific Officer, Head of Research Strategy & Alliances
Solve M.E.
Glendale, CA 91206
Klimas, Nancy, MD
Director, Institute for Neuro-Immune Medicine
Nova Southeastern University
Fort Lauderdale, FL 33328
Nacul, Luis, MBBS, PhD
Clinical Associate Professor
London School of Hygiene and Tropical Medicine
London, United Kingdom
Mangalathu Rajeevan, PhD
Microbiologist
Centers for Disease Control and Prevention
Atlanta, GA 30333
Unger, Elizabeth, MD
Chief, Chronic Viral Diseases Branch, Centers for Disease Control and Prevention
Atlanta, GA 30333
Please note that your application will be shared with BRAC members, NINDS program staff, and BioSEND staff. Access and review of all applications is guided ethical research standards, as described in the Confidentiality Agreement.
Cellular Circadian Rhythm Disruption in ME/CFS
Michael McCarthy, University of California – San Diego/VA San Diego Healthcare Research Service
Cohort: Chronic Fatigue Initiative (CFI)
Review Date: 2021
Abstract: We hypothesize that TGF-β signaling is upregulated in ME/CFS and remains persistently elevated leading to a series of pathological events including circadian rhythm disruption that contributes to sleep disruption and cognitive complaints in a subset of ME/CFS patients. We anticipate that serum from ME/CFS patients with significant sleep disruption will be sufficient to cause circadian disruption in cultured fibroblasts and neurons. Our laboratory has substantial experience performing cellular circadian rhythm assays and has extensively used the NIH 3T3 cell model with Per2-luc transfection. In this aim, the effects on rhythms of serum from ME/CFS patients and control will be studied using Per2-luc in fibroblasts to determine if there are disease-specific factors (such as TGF-β) that affect cellular rhythms in live cells. In multi-day cellular rhythm assays using live cells, we will identify and characterize ME/CFS-associated abnormalities, identify the serum factors responsible, and assess the role of TGF-β using gene expression knockdown, recombinant cytokines, and pharmacological interventions to recapitulate or block the effects of serum.
Autoantibodies Against Chemokines in CFS/ME
Davide Robbiani, Università della Svizzera italiana
Cohort: Chronic Fatigue Initiative (CFI)
Review Date: Pilot analysis, 2022; Expanded analysis 2023
Abstract: The primary aim of this pilot study is to measure the level of plasma autoantibodies against the 43 human chemokines in CFS/ME patients. This will be compared to matched cohort controls, and to convalescent individuals after COVID-19 (with or without long-COVID) and other infections. Moreover, as a secondary aim, we will test the hypothesis that common cold coronaviruses may be involved in CFS/ME pathogenesis by measuring the same samples for the presence of antibodies to the spike protein of human common cold coronaviruses (229E, OC43, NL63, HKU1) and SARS-CoV-2. Since the presence of specific anti-chemokine antibodies is associated with protection from long-COVID, in addition to having diagnostic utility, the study of these autoantibodies in CFS/ME has the potential to pave the way to novel therapeutic approaches.
Sluss MECFS NINDS Research Strategy
Hayla Sluss, University of Massachusetts Chan Medical School
Cohort: Chronic Fatigue Initiative (CFI)
Review Date: 2024
Abstract: A correlate of ME/CFS disease is the presence of vascular endothelial cell dysfunction that may contribute to pathogenesis. Endothelial cell dysfunction in ME/CFS has been characterized by decreased eNOS activity and production of nitric oxide (NO), endothelial cell senescence, and increased permeability of the intestinal and blood brain barrier that lead to endotoxin-mediated inflammation. This dysfunction has been proposed to be mediated by changes in the serum proteome and metabolome. Evidence to support this conclusion is based on the effects of ME/CFS serum to suppress NO production by endothelial cells. Moreover, ME/CFS plasma, compared with control plasma, promotes endothelial cell senescence. Endothelial dysfunction can lead to impaired blood brain barrier function. In addition, ME/CFS disease is associated with mitochondrial defects that may contribute to disease pathogenesis. This study aims to shed light on the role of endothelial senescence in ME/CFS pathogenesis. Understanding these mechanisms will have important translational implications for developing targeted interventions to improve outcomes in ME/CFS patients.