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Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination
TLDR
At a given time point of the disease, the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient, suggesting that MS may be a disease with heterogeneous pathogenetic mechanisms. Expand
Cortical demyelination and diffuse white matter injury in multiple sclerosis.
TLDR
Global brain pathology in multiple sclerosis is analysed, focusing on the normal-appearing white matter (NAWM) and the cortex, to suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter. Expand
The Immunopathology of Multiple Sclerosis: An Overview
TLDR
Recent evidence is described that the spectrum of MS pathology is much broader, including demyelination in the cortex and deep gray matter nuclei, as well as diffuse injury of the normal‐appearing white matter. Expand
Microglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions
TLDR
Using a panel of bone marrow chimeric and adoptive transfer experiments, it is found that circulating Ly-6ChiCCR2+ monocytes were preferentially recruited to the lesioned brain and differentiated into microglia. Expand
Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway.
TLDR
The ability of dimethylfumarate to activate nuclear factor (erythroid-derived 2)-related factor 2 may offer a novel cytoprotective modality that further augments the natural antioxidant responses in multiple sclerosis tissue and is not yet targeted by other multiple sclerosis therapies. Expand
Clinical and radiographic spectrum of pathologically confirmed tumefactive multiple sclerosis
TLDR
Although lesion size >5 cm was associated with a slightly higher EDSS at last follow-up, long-term prognosis in patients with disease duration >10 years was better compared with a population-based multiple sclerosis cohort matched for disease duration (EDSS 3.5; P < 0.001). Expand
A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis
TLDR
In vivo imaging and pharmacological experiments show that macrophage-derived reactive oxygen and nitrogen species (ROS and RNS) can trigger mitochondrial pathology and initiate FAD, and suggest that inflammatory axon damage might be spontaneously reversible and thus a potential target for therapy. Expand
Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time.
TLDR
The results indicate that a putative axon-protective treatment should start as early as possible and include strategies preventing T cell/macrophage-mediated axon destruction and leading to remyelination of axons. Expand
Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous system.
TLDR
Elevated interferon beta concentrations in the CNS, but not blood, of mice with experimental autoimmune encephalomyelitis, a model for CNS autoimmunity are demonstrated, indicating a distinct protective function of type I IFNs during autoimmune inflammation of the CNS. Expand
Inflammatory cortical demyelination in early multiple sclerosis.
TLDR
In this cohort of patients with early-stage multiple sclerosis, cortical demyelinating lesions were frequent, inflammatory, and strongly associated with meningeal inflammation. Expand
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