The goal of this observational study is to assess the clinical response and the effect of autophagy function in ME/CFS patients before, during and throughout oral low dose sirolimus (rapamycin) therapy. The main questions this study aims to answer are:
Does rapamycin reduce the overall symptom burden of ME/CFS and does it improve the quality of life?
Does rapamycin change mTOR driven autophagy deficits observed in a subset of ME/CFS patients?
Participants will be asked to complete a series of questionnaires and quality of life instruments before starting rapamycin therapy prescribed by their physician and throughout their course of treatment. Study blood samples will be collected before starting therapy and throughout the course of treatment to assess serological markers of autophagy.

开始日期2023-12-11

申办/合作机构

Simmaron Research, Inc.

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2023-04-24·Infectious agents and cancer

Correction: Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases.

作者: Peterson, Daniel ; Roy, Avik ; Knox, Konstance ; Armstrong, Jan ; Gottschalk, Carl Gunnar

2016-02-01·Molecular Psychiatry1区 · 医学

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

1区 · 医学

Article

作者: Gottschalk, G ; Peterson, D L ; Hornig, M ; Knox, K K ; Schultz, A F ; Che, X ; Lipkin, W I ; Eddy, M L

Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.

2015-01-01·Mediators of Inflammation3区 · 医学

Cytokines in the Cerebrospinal Fluids of Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

3区 · 医学

ArticleOA

作者: Marshall-Gradisnik, S ; Gottschalk, G ; Staines, D ; Nguyen, T ; Peterson, D ; Ramos, S ; Brenu, E W

Objectives. Previous research has provided evidence for dysregulation in peripheral cytokines in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). To date only one study has examined cytokines in cerebrospinal fluid (CSF) samples of CFS/ME patients. The purpose of this pilot study was to examine the role of cytokines in CSF of CFS/ME patients. Methods. CSF was collected from 18 CFS/ME patients and 5 healthy controls. The CSF samples were examined for the expression of 27 cytokines (interleukin‐ (IL‐) 1β, IL‐1ra, IL‐2, IL‐4, IL‐6, IL‐7, IL‐8, IL‐9, IL‐10, IL‐12p70, IL‐13, IL‐15, IL‐17, basic FGF, eotaxin, G‐CSF, GM‐CSF, IFN‐γ, IP‐10, MCP‐1 (MCAF), MIP‐1α, MIP‐1β, PDGF‐BB, RANTES, TNF‐α, and VEGF) using the Bio‐Plex Human Cytokine 27‐plex Assay. Results. Of the 27 cytokines examined, only IL‐10 was significantly reduced in the CFS/ME patients in comparison to the controls. Conclusions. This preliminary investigation suggests that perturbations in inflammatory cytokines in the CSF of CFS/ME patients may contribute to the neurological discrepancies observed in CFS/ME.

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