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Deep Assessment of Neuroinflammation

Using CNS Imaging and Analysis of CSF, Blood, Saliva Samples

To explore the hypothesis that low-grade neuroinflammation in the central nervous system can be part of the cardinal symptoms of ME/CFS. This can possibly be monitored in cerebrospinal fluid (CSF) as a result of the inflammatory reaction itself or as secondary markers of cell degradation and impaired cell repair mechanisms. Furthermore, we want to explore if the inflammation could be a result of or lead to increased intracranial pressure and reduced circulation.

  • Jonas Bergquist in collaboration with the OMF supported Harvard Collaboration

Our study will be the first to systematically measure CNS structural abnormalities in a large ME/CFS case-control study using cerebrospinal fluid collection, in-situ measurement of intracranial pressure together with the study of microglia activation (the resident immune cells of the CNS) by the implication of a novel diffusion-based MRI methodology. Added to this will be collected biospecimens to perform extensive state-of-the-art analyses with the ambition to identify diagnostic and prognostic biomarkers.

The analysis of cerebrospinal fluid and matching plasma samples are IRB-approved and already initiated while the IRB review for the use of the novel MRI methodology will kick off shortly.

STUDY HYPOTHESIS AND DESCRIPTION

In Professor Jonas Bergquist’s laboratory, they have studied neuroinflammation and neurodegeneration for over three decades, and especially the in-depth analysis of cerebrospinal fluid has been a specialty. In 2010, the first evidence of low-grade inflammation was presented in ME/CFS patients and has since then been part of the focus for the continuous search of the pathomechanism underlying the disease. In the last couple of years, Professor Bergquist has been the supervisor of Björn Bragée (MD and head of the Bragée Clinic, Stockholm) and has been investigating, in close collaboration, the molecular features of cerebrospinal fluid from ME/CFS patients.

The overall aim is to explore the hypothesis that low-grade neuroinflammation, microglia activation, deranged flow of the cerebrospinal fluid (CSF), and deranged intracranial pressure (ICP) could explain the cardinal symptoms of ME/CFS. If this hypothesis proves true, it opens a new research area in ME/CFS and hopes for effective treatment to reduce neuroinflammation, regulate ICP, and relieve symptoms associated with ME/CFS. This study will make use of CNS imaging and analysis of CSF and blood samples and will identify proteomic and metabolomic biomarkers of the disease, a highly needed tool in the diagnostic and prognostic process. Through a combination of more detailed clinical examination, evaluation, and multiOmics biomarker analysis, we will be able to provide more individually adapted care and, hopefully, a cure.

OBJECTIVES

Graphic showing how proinflamatory cytokines and damage to blood brain barrier

  • Characterize neuroinflammation by CSF composition analyses, monitoring inflammatory markers, as well as markers of cell damage and impaired cell repair mechanisms.
  • Characterize the prevalence and severity of CNS structural abnormalities and microglia activation using structural and diffusion-based magnetic resonance imaging (MRI).
  • Characterize CSF pressure and flow using noninvasive and invasive techniques during lumbar puncture.
  • Identify biomarkers of the disease by extensive and detailed analyses of CSF and blood using proteomics and metabolomics.
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME / CFS) Post Treatment Lyme Disease Syndrome (PTLDS), Fibromyalgia Leading Research. Delivering Hope.Open Medicine Foundation®

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