Multiple sclerosis--the plaque and its pathogenesis.

By E. Frohman, M. Racke, C. Raine. New England Journal of Medicine, 2006

1,763 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/de3521817413543f7fddbb4a8d14ad69cae86e68

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Hans Lassmann
2. R. Kaufman
3. F. Aloisi
4. R. Ransohoff

In Pathology and Forensic Medicine

1. Hans Lassmann
2. Wolfgang Brück
3. C. Lucchinetti
4. Robin J. M. Franklin
5. F. Aloisi
6. R. Ransohoff

Citations in the corpus

• The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “Multiple sclerosis (MS) is a neuro-in fl ammatory, slowly progressing and invalidating disease affecting 0.05% – 0.15% of Caucasians [94], mostly young adults, hence with a considerable social and economic impact [95].”
• The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “Thus, it was suggested that remyelination, occurring at the early stages of MS, is unstable (35).”
• Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS. (2009, background): “…be extensive in MS (Patrikios et al. 2006; Patani et al. 2007), it is an inconsistent event, and the accumulated load of lesions that fail to remyelinate in a timely manner contributes to irreversible axon loss and progressive neurological deterioration (Frohman et al. 2006; Trapp and Nave 2008).”
• Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “…Denmark and 6Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA Correspondence to: Prof. Dr Hans Lassmann, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Wien, Austria E-mail: hans.lassmann@meduniwien.ac.at Although spontaneous remyelination does…”
• Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. (2007, background): “…models of multiple sclerosis favour a doi:10.1093/brain/awm038 Brain (2007), 130, 1089^1104 T-cell-mediated pathogenesis, an important role for humoral immunity in the development of multiple sclerosis lesions is also recognized (Sospedra and Martin, 2005; Owens et al., 2006; Frohman et al., 2006).”
• MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis (2009, background): “As a prototype of organ-specific autoimmune disease, multiple sclerosis is manifested by chronic inflammatory demyelination of the central nervous system (CNS) and is one of the foremost causes of nontraumatic neurological disability in young adult”
• From endoplasmic-reticulum stress to the inflammatory response (2008, background): “Multiple sclerosis is a neurodegenerative disease that is marked by demyelination, oligodendrocyte loss and T-cell activation associated with IFN-γ productio”
• Mechanisms Underlying Inflammation in Neurodegeneration (2010, neutral): “The deposition of antibodies and complement around demyelinated lesions (Frohman et al., 2006) and axonal degeneration in the progression phase of MS have also been observed (Trapp and Nave, 2008).”