Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions.

By B. Kornek, M. Storch, Robert Weissert, E. Wallstroem, A. Stefferl, T. Olsson, C. Linington, M. Schmidbauer, Hans Lassmann. American Journal of Pathology, 2000

962 citations recorded by the source corpus.

Subfields: Neurology, Pathology and Forensic Medicine, Rheumatology

View Paper: https://www.semanticscholar.org/paper/8be737a0b232e9398caa4d6971dbd568d9c1f2bf

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Citations in the corpus

Oxidative damage in multiple sclerosis lesions (2011, background): “, 2009) and close contacts between activated microglia or macrophages and degenerating axons, myelin sheaths and oligodendrocytes have been described (Ferguson et al., 1997; Trapp et al., 1998; Kornek et al., 2000).”
Multiple Sclerosis Pathology. (2018, background): “Importantly, there is a low degree of ongoing acute axonal injury, reflected by the disturbance of fast axonal transport also in inactive lesions, indicating the ongoing demise of chronically demyelinated axons (Kornek et al. 2000).”
Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time. (2002, background): “A variety of different histopathological studies exist that investigated acute axonal damage in multiple sclerosis (Ferguson et al., 1997; Trapp et al., 1998; Bitsch et al., 2000; Kornek et al., 2000).”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “…oligodendrocyte susceptibility Chronic EAE in CNTF-deficient mice sensitized with MOG 35-55 Linker et al. (2002) Axonal injury in demyelinated plaques All chronic EAE models in mice and rats Kornek et al. (2000) Cortical demyelination Recombinant MOG 1–125 induced EAE in marmosets or in LEW 1.”
Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS) (2011, background): “Optic neuritis, often a first sign of autoimmune demyelination, has also been modelled (Rao et al., 1977; Raine et al., 1980; Mendel et al., 1995; Kornek et al., 2000; Pomeroy et al., 2005; Gold et al., 2006) ‘Active’ EAE is induced by immunization with CNS tissue or myelin peptides, such as myelin…”
Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “Other characteristic features of shadow plaques were a moderate reduction of axonal density (Kornek et al., 2000), the absence of macrophages with early myelin degradation products (Fig.”
The relation between inflammation and neurodegeneration in multiple sclerosis brains (2009, background): “The above mentioned studies do not exclude the possibility that a diffuse inflammatory process in inactive lesions, the NAWM, the cortex or the meninges may ultimately drive neurodegeneration at these sites (Kornek et al., 2000; Kutzelnigg et al., 2005; Magliozzi et al., 2007).”
Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. (2007, background): “Axon loss in WML has been linked with inflammatory episodes occurring during relapses, in addition to a longer term slower loss that is thought to predominate during the progressive phase (Trapp et al., 1998; Kornek et al., 2000).”
The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “The concept that progressive (‘‘slow-burning’’) axonal loss occurring over time in demyelinated lesions is responsible for late chronic disability is supported by histologic studies (Bjartmar et al., 2000; Kornek et al., 2000) and by serial MRI studies revealing accelerated atrophy over time (Lossef”
The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “As chronic demyelination is associated with slowly progressive axonal loss (49), stimulation of remyelination by growth factors or through (stem) cell transplantation is considered an attractive therapeutic option in MS patients.”
Clinical and Pathological Insights into the Dynamic Nature of the White Matter Multiple Sclerosis Plaque (2015, background): “The presence of tissue atrophy secondary to ongoing axonal degeneration and loss within the inactive plaque center may, with time, counterbalance plaque expansion at the smoldering plaque edge.(34) Therefore, in advanced stages of MS, plaque size by MRI might not increase per se, and the overall vol”