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Demyelination is the cause of disability in various neurological disorders. It is therefore crucial to understand the molecular regulation of oligodendrocytes, the myelin forming cells in the CNS. Growth factors are known to be essential for the development and maintenance of oligodendrocytes and are involved in the regulation of glial responses in various(More)
Recent evidence suggests that astrocytes play an important role in regulating de- and remyelination in multiple sclerosis. The role of astrocytes is controversial, and both beneficial as well as detrimental effects are being discussed. We performed loss-of-function studies based on astrocyte depletion in a cuprizone-induced rodent model of demyelination.(More)
Microglia play a key role in the initiation and perpetuation of de- and remyelination because of their ability to present antigens and clear cell debris by phagocytosis. Different factors expressed or secreted by microglia seem to play an important role in regenerative processes. But it remains unclear which factors lead to a protective microglial phenotype(More)
Apart from their involvement in the pathogenesis of demyelinating diseases such as multiple sclerosis, there is emerging evidence that matrix metalloproteinases (MMPs) also promote remyelination. We investigated region-specific expression patterns of 11 MMPs and 4 tissueinhibitors of metalloproteinases (TIMPs) in the cuprizone murine demyelination model.(More)
Demyelinating optic neuritis (ON) is the most common cause of optic neuropathy typically presenting with a subacute painful visual loss. In 20% of patients with multiple sclerosis (MS), ON is the presenting symptom and half of the patients with isolated ON develop MS within 15 years. The diagnosis of ON plays an important role in neurological practice. A(More)
Beside its effects on T cells, a direct influence on cells of the myelo-monocytic lineage by GA becomes evident. Recently, we demonstrated that GA drives microglia to adopt properties of type II antigen presenting cells (APC) and increases their phagocytic activity. In the present work, we focused on human blood monocytes in order to examine whether GA may(More)
Glatiramer acetate (GA) is an approved immunomodulating agent for the treatment of relapsing–remitting multiple sclerosis. Its mode of action is attributed to a T helper cell-type 1 (Th1) to Th2 cytokine shift in T cells. Th2-type GA-reactive T cells migrate into the brain and act suppressive at the sites of inflammation. However, there is increasing(More)
Longitudinal extensive transverse myelitis (LETM) is defined as a spinal cord lesion that extends over three or more vertebrae, as seen on MRI of the spine. The clinical presentation of a patient with LETM is often dramatic and can consist of paraparesis or tetraparesis, sensory disturbances, and gait, bladder, bowel and/or sexual dysfunction. LETM is a(More)
Background: Pathogenic autoantibodies targeting the recently identified leucine rich glioma inactivated 1 protein and the subunit 1 of the N-methyl-D-aspartate receptor induce autoimmune encephalitis. A comparison of brain metabolic patterns in F-fluoro-2-deoxy-d-glucose positron emission tomography of anti-leucine rich glioma inactivated 1 protein and(More)
In multiple sclerosis (MS) matrix metalloproteinases (MMP) are believed to be involved in the disruption of the blood brain barrier and demyelination. MMP-9 is increased in the cerebrospinal fluid of MS patients and expressed in MS lesions, indicating an involvement in MS pathogenesis. It is known that activated microglia secrete MMP. Modulation of MMP may(More)