News

Mon, 03/06/2019
Publication: Teriflunomide treatment for multiple sclerosis modulates T cell mitochondrial respiration with affinity-dependent effects.
Muenster. For the first time scientists from the University of Münster could show that multiple sclerosis (MS) alters the energy metabolism of T cells during acute phases of disease exacerbation. Therapeutic interventions targeting the metabolism of activated T cells display new potential avenues for treatment of patients with MS affecting around 250,000 people in Germany. The […]...more
Mon, 29/04/2019
Publication: Calcium influx through plasma-membrane nanoruptures drives axon degeneration in a model of multiple sclerosis.
Munich.  Here SFB researchers from Munich use in vivo calcium imaging in a multiple sclerosis model to show that cytoplasmic calcium levels determine the choice between axon loss and survival. Calcium can enter the axon through nanoscale ruptures of the axonal plasma membrane that are induced in inflammatory lesions. Neuron doi: 10.1016/ j.neuron.2018.12.023...more
Tue, 04/12/2018
SFB 128 International Symposium
SFB 128. We are happy to announce the international Symposium of the Collaborative Research Centre 128 “Multiple Sclerosis” taking place from Sunday, September 15th, till Tuesday, September 17th, 2019 in the Rhine Main region. Full details of the event will follow....more


Wed, 23/11/2016 | Featured publication: Imaging matrix metalloproteinase activity in multiple sclerosis as a specific marker of leukocyte penetration of the blood-brain barrier

Münster – The enzymes gelatinase A/matrix metalloproteinase-2 (MMP-2) and gelatinase B/MMP-9 are essential for induction of neuroinflammatory symptoms in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). In the absence of these enzymes, the disease does not develop. SFB128 scientists of Prof. Dr. Lydia Sorokin’s group, therefore, investigated the cellular sources and relative contributions of MMP-2 and MMP-9 to disease at early stages of EAE induction. They demonstrated that MMP-9 from an immune cell source is required in EAE for initial infiltration of leukocytes into the central nervous system and that MMP-9 activity is a reliable marker of leukocyte penetration of the blood-brain barrier.
The neuroscientists then developed a molecular imaging method to visualize MMP activity in the brain using fluorescent- and radioactive-labeled MMP inhibitors (MMPis).
By using radioactive MMP ligand in EAE animals the Muenster neuroscientists produced positron emission tomography (PET) images of MMP activity in patients with MS.
In contrast to traditional T1-gadolinium contrast-enhanced MRI, MMPi-PET enabled tracking of MMP activity as a unique feature of early lesions and ongoing leukocyte infiltration.
MMPi-PET therefore allows monitoring of the early steps of MS development and provides sensitive, noninvasive means of following lesion formation and resolution in murine EAE and human MS, the neuroscientists conclude. Their work was part of the SFB projects B03 and Z02.