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CRC-TR-128: Initiating/Effector Versus Regulatory Mechanisms In Multiple Sclerosis - Progress Towards Tackling the Disease

Laufzeit: 01.01.2020 - 31.12.2024

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Kurzfassung


Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disease of the central nervous system (CNS). Currently, no cure is available. Although therapeutic options have improved during the last years, many open questions still remain regarding the determinants of disability progres-sion and disease susceptibility, initiation, perpetuation and phenotype variation, and especially individual predictability. This CRC elucidates the complex crosstalk between the immune and the nervous...Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disease of the central nervous system (CNS). Currently, no cure is available. Although therapeutic options have improved during the last years, many open questions still remain regarding the determinants of disability progres-sion and disease susceptibility, initiation, perpetuation and phenotype variation, and especially individual predictability. This CRC elucidates the complex crosstalk between the immune and the nervous system at molecular, cellular, and systems biology levels, using a highly interdisciplinary and translational approach.
 
The vision for this third funding period is to contribute to the development of pathomechanistic knowledge and patient-relevant deliverables to help drive the worldwide search for prognostic and therapeutic improvement in the field of multiple sclerosis, and thus neuroimmunology.


  • A03: Interplay between pro-inflammatory cytokines and chromatin-remodeling en-zymes in the regulation of central nervous system de-myelination and repair (Waisman, Jacob)

  • A07: Role of IL-6 in shaping local immune milieus in the CNS (Waisman)

  • A08: Impact of diet and intestinal microbiota on the gut-CNS-axis –implications for CNS autoimmunity (Schuppan)

  • B04: Unraveling the role of mye-loid cells and metabolism in clinical progression of MS (Bittner, Bopp)

  • B05: Topological patterns of damage and compensation in chronic neuroinflammation (Groppa)

  • B09: Topological patterns of damage and compensation in chronic neuroinflammation (Ellwardt, Stroh)

  • B12: Balancing glutamate and cation channel signaling in inflammatory neuronal injury (Bittner)

  • B14: NfL and EGFL7 as biomarkers for neuroaxonal damage and BBB-integrity in neuroinflammation: A translational approach (Uphaus, Zipp)

  • B15: Spatiotemporal effects of IL-4 on CNS repair during neuroinflammation (Vogelaar, Zipp)

  • Z02: Clinical translational Unit (Lüssi, Fleischer)

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