Gottschalk, Gunnar, Peterson, Daniel, Knox, Konstance et al. · Molecular and cellular neurosciences · 2022 · DOI
Researchers found that people with ME/CFS have higher levels of a protein called ATG13 in their blood compared to healthy people. When they tested this protein on brain immune cells in the lab, it triggered the production of harmful molecules called free radicals (oxidative stress). This suggests that a breakdown in the body's cellular recycling system (autophagy) might contribute to the inflammation and stress response seen in ME/CFS.
This study identifies a specific molecular pathway—ATG13-RAGE signaling in microglial cells—that may explain how brain inflammation develops in ME/CFS. Understanding this mechanism could open new avenues for targeted treatments and biomarker development, potentially offering patients therapeutic options beyond symptom management.
This study does not prove that ATG13 is the primary cause of ME/CFS or that blocking ATG13 will treat the disease in patients. It is an in vitro laboratory study, so findings may not translate directly to what happens in living patients. The study shows correlation and a possible mechanism, but clinical trials would be needed to establish whether targeting this pathway benefits patients.
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
Gottschalk, Gunnar, Peterson, Daniel, Knox, Konstance, Maynard, Marco, Whelan, Ryan J, & Roy, Avik (2022). Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE).. Molecular and cellular neurosciences. https://doi.org/10.1016/j.mcn.2022.103731
BibTeX
@article{mecfsatlas-gottschalk-2022-elevated-atg13,
author = {Gottschalk, Gunnar and Peterson, Daniel and Knox, Konstance and Maynard, Marco and Whelan, Ryan J and Roy, Avik},
title = {Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE).},
journal = {Molecular and cellular neurosciences},
year = {2022},
doi = {10.1016/j.mcn.2022.103731},
note = {PubMed: 35487443},
url = {https://www.mecfsatlas.com/evidence/gottschalk-2022-elevated-atg13},
}Atlas snapshot reference
ME/CFS Atlas. Generator v1 / Scanner v1.4 / policy v0.1. Accessed 2026-05-26. https://www.mecfsatlas.com/evidence/gottschalk-2022-elevated-atg13
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