Journal of IiMER May 2025 Felipe Correa-da-Silva (Netherlands Institute for Neuroscience, Netherlands) BRMEC14: Delineating Clinical Phenotypes and HPA-Axis Dysfunction in ME Dr Felipe Correa-da-Silva is a postdoctoral researcher at the Netherlands Institute for Neuroscience. His work centres on molecular biology and neuroendocrinology, particularly the role of neuron-glia interactions and hypothalamic function in disease. He has a strong interest in the hypothalamic-pituitary-adrenal (HPA) axis and its dysfunction in ME/CFS, exploring how this contributes to clinical phenotypes and symptom variability. His research aims to delineate subgroups within ME/CFS by combining clinical phenotyping with biological measures, supporting the development of more targeted and personalised treatment approaches. Dr Correa-da-Silva is also involved in the Netherlands Brain Bank’s ME/CFS donor programme, advancing research into the neurological aspects of ME/CFS. At BRMEC14, he will discuss how clinical phenotyping and HPA axis evaluation can help define distinct ME/CFS subgroups, facilitating more precise research and treatment strategies. Maxim N. Artyomov and Tomas Paulenda (Washington University in St. Louis, USA) BRMEC14: Itaconate modulates immune responses via inhibition of Peroxiredoxin 5 Professor Maxim N. Artyomov and Dr Tomas Paulenda are leading researchers in immunometabolism and systems immunology. Their recent work demonstrates that itaconate-a metabolite produced during inflammation-inhibits peroxiredoxin 5 (PRDX5), an antioxidant enzyme critical for managing mitochondrial oxidative stress in immune cells. This non-covalent inhibition alters mitochondrial peroxide levels and the redox environment in activated macrophages, significantly affecting immune signalling pathways and fine-tuning inflammatory responses. This discovery builds on Artyomov’s earlier work exploring itaconate’s role in modulating macrophage behaviour and inflammation. In light of their recent important research, the charity is delighted to announce the addition of Maxim N. Artyomov and Tomas Paulenda to the BRMEC14 programme. These findings are highly relevant to ME, a condition marked by immune dysregulation, mitochondrial dysfunction, and persistent oxidative stress. The study links itaconate’s regulation of mitochondrial redox balance to mechanisms often impaired in ME, suggesting that by inhibiting PRDX5, itaconate may influence the handling of reactive oxygen species in immune cells. This could contribute to the mitochondrial dysfunction and abnormal oxidative stress observed in ME patients. Invest in ME Research Page 21 of 43
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