{"id":4368,"date":"2025-03-26T17:00:24","date_gmt":"2025-03-26T16:00:24","guid":{"rendered":"https:\/\/www.sfb274.de\/?p=4368"},"modified":"2025-04-08T11:33:26","modified_gmt":"2025-04-08T09:33:26","slug":"symposium-34-gns-2025","status":"publish","type":"post","link":"https:\/\/www.sfb274.de\/en\/symposium-34-gns-2025\/","title":{"rendered":"TRR 274 at the German Neuroscience Society 2025"},"content":{"rendered":"\n

Symposium 34: Modelling CNS recovery from autoimmune neurodegeneration<\/strong><\/h2>\n\n\n\n

Saturday, March 29, 11:30 – 13:30<\/em><\/p>\n\n\n\n

Chairs: Alexander Fl\u00fcgel<\/mark><\/strong> and Djordje Miljkovi\u0107<\/strong>, Goettingen and Belgrade (Serbia)<\/p>\n\n\n\n

Multiple sclerosis, neuromyelitis optica spectrum disorder (NMOSD) and MOG antibody-associated diseases (MOGAD) are autoimmune diseases of the CNS. They are characterized by chronic inflammation of the nervous tissue, which regularly leads to irreversible structural damage of the central nervous system. Typical of these diseases are a destruction of the myelin, a disturbance in neuronal processes and ultimately progressive, (currently) irreversible neurodegeneration. While some fundamentals of the inflammatory pathogenesis of the diseases are already understood and several therapeutic strategies have been developed to curb the inflammation, it has so far been difficult to influence the progressive destruction of the neuronal tissue. An essential key to the development of therapeutic neuroprotective approaches is the inclusion of appropriate experimental models. Scientists working on such models will present their data at this symposium. The aim of their studies is to define checkpoints which determine the transition of the CNS inflammation to neurodegeneration and hereby to develop preventive strategies or to trigger regeneration of the injured CNS tissue. The symposium gave researchers interested in this field of neuroscience the opportunity to discuss the possibilities of improving current approaches to studying neurodegeneration in animal models of chronic autoimmune CNS diseases.<\/p>\n\n\n\n

Schedule:<\/strong><\/p>\n\n\n\n