Drosen, Molly E, Bulbule, Sarojini, Gottschalk, Gunnar et al. · Immunologic research · 2025 · DOI
Researchers gave mice a drug that overactivates a protein called mTOR and found it triggered muscle weakness, nerve damage, and worsening fatigue after exercise—similar to post-exertional malaise (PEM) in ME/CFS. The drug blocked a cellular cleanup system called autophagy, which led to inflammation and damage to the nerves controlling muscles. Mice engineered to have impaired autophagy showed similar problems, suggesting that broken autophagy may be involved in ME/CFS fatigue and exercise intolerance.
This study identifies a potential molecular mechanism linking autophagy dysfunction to both chronic muscle weakness and post-exertional malaise—two hallmark features of ME/CFS. Understanding that mTOR hyperactivation may impair cellular cleanup and trigger demyelination and inflammation offers new targets for therapeutic intervention in ME/CFS patients.
This study does not prove that mTOR hyperactivation or ATG13 impairment occurs in human ME/CFS patients; these are animal models that may not fully recapitulate the human disease. It also does not establish causality in humans or rule out other contributing genetic and environmental factors in ME/CFS pathogenesis. Results in mice do not guarantee efficacy or safety of mTOR-targeting treatments in clinical practice.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
The first block is for the primary paper and is the citation you should use in research work. The atlas-snapshot line only applies if you are specifically referring to this atlas’s reading of the paper on the date shown.
Primary citation
Drosen, Molly E, Bulbule, Sarojini, Gottschalk, Gunnar, Peterson, Daniel, Allen, Linda Adrienne, Arnold, Leggy A, et al. (2025). Inactivation of ATG13 stimulates chronic demyelinating pathologies in muscle-serving nerves and spinal cord.. Immunologic research. https://doi.org/10.1007/s12026-024-09557-7
BibTeX
@article{mecfsatlas-drosen-2025-inactivation-atg13,
author = {Drosen, Molly E and Bulbule, Sarojini and Gottschalk, Gunnar and Peterson, Daniel and Allen, Linda Adrienne and Arnold, Leggy A and Roy, Avik},
title = {Inactivation of ATG13 stimulates chronic demyelinating pathologies in muscle-serving nerves and spinal cord.},
journal = {Immunologic research},
year = {2025},
doi = {10.1007/s12026-024-09557-7},
note = {PubMed: 39777574},
url = {https://www.mecfsatlas.com/evidence/drosen-2025-inactivation-atg13},
}Atlas snapshot reference
ME/CFS Atlas. Generator v1 / Scanner v1.4 / policy v0.1. Accessed 2026-05-27. https://www.mecfsatlas.com/evidence/drosen-2025-inactivation-atg13
Contribute
Private, reviewed by a human. Not a public comment thread.