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Linking brain blood flow, neuroinflammation, metabolism and hormones in ME, POTS and Long COVID

Study AIM

The study will explore the structural, neuro-vascular, and biochemical differences in the brains of individuals with ME/CFS, Long COVID, and POTS to elucidate the underlying pathology and identify potential targets for effective treatment strategies.

INVESTIGATORS
  • Xiaoyun Wang, PhD
  • Elena Christopoulos
  • Natalie Thomas, PhD
  • David Fineberg, MBBS, FRACGP, DCH
  • Paul Gooley, PhD
  • Leigh Johnston, PhD
  • Rebecca Glarin, BApSc, PGDip(MRI)
  • Rob Williams
  • Bradford Moffat, PhD
  • Christopher Rowe, BMBS, FRACP, MD, FAANMS
  • Christopher Armstrong, PhD
Updates and Potential
  • Recruitment is beginning, and we are expecting it to be completed by the end of 2025.
  • Forming a collaboration with Michelle James for follow up work.
  • Writing paper on glutamate neurotransmitters and enzymes in collaboration with PrecisionLife.
STUDY HYPOTHESIS AND DESCRIPTION

Emerging evidence suggests a potential link between ME/CFS and Long COVID, characterised by similar symptomatology. Additionally, POTS frequently co-occurs with ME/CFS and LC, further complicating symptom management and reducing patients’ quality of life.

Neuroinflammation has recently gained attention as a potential mechanism underlying ME/CFS and LC, with proposed pathways involving sustained glial activation and hypothalamic neuroinflammation. Glutamate dysregulation in the central nervous system, possibly exacerbated by neuroinflammation, may contribute to neuroendocrine dysfunction observed in ME/CFS and LC. Furthermore, reduced brain blood flow could be central to all 3 conditions.

This study aims to investigate brain structural, neuro-vascular, and biochemical differences between groups to deepen our understanding of ME/CFS, LC and POTS pathology and develop effective treatments. By examining astrocyte activity, metabolic variations, cerebral blood flow responses to exercise, and neuroinflammatory markers, we seek to uncover key mechanisms driving ME/CFS symptoms and identify potential therapeutic targets.

OBJECTIVES

  1. Investigate astrocyte activity and glucose hypometabolic patterns to elucidate brain neuroinflammation mechanisms in ME/CFS and LC.
  2. Analyze metabolite variations, particularly glutamate and GABA levels, in the hypothalamus among ME/CFS and LC patients compared to controls.
  3. Explore correlations with central nervous system neuroinflammation, blood hormone levels, and symptom manifestation.
  4. Assess changes in cerebral blood flow during exercise in ME/CFS and POTS patients, both globally and regionally in the brain. Investigate potential synergistic effects in individuals with comorbid ME/CFS and POTS.
  5. Evaluate the impact of cerebral blood flow alterations on symptomatology and post-exertional malaise severity in ME/CFS, LC and POTS populations.

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