Roy lab

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Our team @RedefiningMECFS @ggottschalkPhD continues to perform ground-breaking research in decoding the role of ATG13 in chronic inflammation and now our new research (Toriola M et.al.) is now published in @SpringerNature’s Q1 immunology journal Inflammation Research. doi.org/10.1007/s00011…  Background: CD40 is a key surface antigen expressed on macrophages and other myeloid cells, where it plays a central role in innate immunity by sustaining their inflammatory phenotype. In our earlier study (Immunologic Res 2025) , we demonstrated that the impaired autophagy can trigger sub-threshold infiltration of CD40-immunoreactive macrophages into the vasculature of skeletal muscle tissue. This infiltration contributes to chronic inflammatory changes affecting muscle-serving nerve fibers. Findings: In our current work, we delineate the underlying mechanism. We demonstrate that the genetic depletion of atg13 gene and the subsequent autophagy impairment may initiate a series of metabolic changes in myeloid cells. These changes start with the deficit in mitochondrial energy metabolism (confirmed by Seahorse analyses of OXPHOS and glycolysis), then the augmentation of reactive oxygen species ( Mito-ROS assay), then the nifrosylative inactivation of cellular deacetylase enzyme called SIRT1 , which maintains the acetylation status of NF-κB. These series of metabolic changes drive the induction of the inflammatory phenotype in perivascular macrophages. Along with CD40, we examined the impact of atg13-dependent autophagy impairment in the expressions of other surface antigens such as CD86, CD163, and CD206 in the context of inflammatory response in myeloid cells. Summary: The pathway we describe highlights how NF-kB-mediated inflammatory changes in myeloid cells may contribute to the neurogenic symptoms of muscle fatigue, post-exertional malaise, and potentially post-infectious fatigue syndromes. @MECFSNews @UWM

Excited to contribute a research with @RedefiningMECFS, @ggottschalkPhD on ATG13's role in chronic fatigue, recently accepted by Inflammation Research of @SpringerNature.. The full paper is under production now. Our research is timely and relevant as another study in Nature Communications (Hu et al. PMID: 41309545) linked  ATG13-binding protein FIP200 in long COVID genetics. @MECFSResearch @PlzSolveCFS @MEResearchUK @UWM

Simmaron @RedefiningMECFS @ggottschalkPhD is excited for the early preclinical results of our small molecule-inhibitors SIMMPYRA-1 and 2 to modulate STAT signaling events in reducing chronic inflammation associated with mononucleosis and cytokine upregulations.@BCRFcure @PlzSolveCFS

@thebfrpros Thanks.

@ProfAvikRoy Congratulations.

Rapamycin, a potent inhibitor of mTOR, has been studied for its role as an autophagy inducer and also in immuno rejuvination. Its been approved by FDA for its application in cardiac restenosis and cancer management. Recently, we launced a decentralized clinical trial for low dose rapamycin in the amelioration of clinical symptoms of ME/CFS. We have some exciting data on the alleviation of clinical symptoms of ME/CFS and improvement of overall autophagy. The trial data has been published in our most recent article in the Journal of Translational Medicine ( Impact factor 8.5). Congrats to Brian T Ruan , the first author, who just left Cornell University to study medicine in Tufts University. Our clinical leaders including @StephanieGrach, David Kaufman, and Lucinda Bateman. Congratulations to @ggottschalkPhD the CEO of @RedefiningMECFS and one of the PIs in this study. @PlzSolveCFS @MECFSResearch @MayoClinic @UWM …nslational-medicine.biomedcentral.com/articles/10.11…

The high resolution analysis is currently being studied to understand the molecular effect of rapamycin. We are identifying fast versus slow drug metabolizers, correlation with history of viral infection, duration, symptom severity and different other factors. The customized treatment is not the most time and cost effective strategy, but may be that analysis will demonstrate the dosing regimen and the treatment window.

@ProfAvikRoy Also, will be learn from this study why certain sufferers would *not* respond to it?

@LarryWeis7 Thank you for your support and interest

@ProfAvikRoy Great work Avik!

@AndrewG76201347 Hear

@AndrewG76201347 Glad to bear from you. We need to hear more from you. Please keep in touch with clinicians.

@PlzSolveCFS @ggottschalkPhD @RedefiningMECFS We are excited to have @PlzSolveCFS by our side and also thankful for your support in this study.

Congrats to @ProfAvikRoy & @ggottschalkPhD (@RedefiningMECFS) and co-authors on their publication in the Journal of Translational Medicine. Solve is proud to have co-funded this important research on #rapamycin. Read our easy-to-understand summary here: ow.ly/UBI650XfLiA

@AndrewG76201347 We heard similar stories from other centers. All data recorded in RedCap digital server maintained by Cornell University scientists. All data was assessed by certified statisticians.

@ProfAvikRoy Thanks! I started Rapamycin based on the preprint of this paper. Currently up to 4mg once per week. Definitely helping, highly physical & cognitive activity limit & most importantly I have not had PEM since I started ~10 weeks ago.

@Pnina3434 Definitely, there may be a gender-biased response. But, the heterogeneous effect does not necessarily depend on gender only. There may be other reasons such as age , duration of the disease, severity of the disease, history, comorbidities, metabolism rate of the drug etc.

@ProfAvikRoy Doesn’t match my experience. I have ME & LC. Worked my way up to 6mg. Gave me a significant boost at first and then wore off. It would be interesting to know male v female responses, cause, anecdotally, I’ve observed the effect is unsustained in women.

@HazylightsSa All reported data was collected from multiple centers , stored in a digital server, and assessed by many clinicians independently.

@ProfAvikRoy Thanks for trialing this but this doesn't really match with what I gathered from anecdotes, the response rate seems to be very high in your study.

Patients with post-infectious fatigue demonstrated significant recovery from PEM symptoms. Although statistically low numbers in our pilot trial as because we have started with few cases, but we have a larger sample size in our phase-II trial and we are getting a strong response.

@ProfAvikRoy Does mister roy think that this treatment may help the covid vax injured???

@MEResearchUK Yes, which plays a key role in ME/CFS pathogenesis.

The Nobel Prize in Physiology or Medicine has been awarded to researchers who discovered regulatory T cells (Tregs). Tregs have been described as "good candidates for the underlying pathology" of ME/CFS. Read more: tinyurl.com/mwz7vnxj

The #UWM community extends its heartfelt sympathies and condolences to the @MarquetteU lacrosse team and the entire Marquette community for the tragic loss of its two student-athletes. We are keeping you in our thoughts.

@ggottschalkPhD @YouTube Great discussion on the current and future treatment options of rapamycin in ME/CFS and other conditions with debilitating fatigue and systemic symptoms.

ME/CFS, Long Covid, and Rapamycin youtu.be/W_aw-DsQiQM?si… via @YouTube Lucky to sit down with David Kaufman and Ilene Ruhoy. Check out the pod here.

The dual seminar featuring MIDD’s scientists @UWM at the Medical College of Wisconsin (MCW) @MCWCancerCenter will be held on August 29th, from 12 noon to 1 PM.

New Pre-pint from our team ⁦⁦@RedefiningMECFS⁩ . Genetic depletion of early autophagy protein ATG13 impairs mitochondrial energy metabolism, increases oxidative stress, and preferentially induces the pro inflammatory M1 phenotype of macrophages. researchsquare.com/article/rs-718…