Hypoxia-like tissue injury as a component of multiple sclerosis lesions.
Recent data suggest that the mechanisms of demyelination and tissue damage in multiple sclerosis (MS) are heterogenous. In this review, evidence is discussed, which show that in a subset of multiple sclerosis patients the central nervous system (CNS) lesions show profound similarities to tissue alterations found in acute white matter stroke, thus suggesting that a hypoxia-like metabolic injury is a pathogenetic component in a subset of inflammatory brain lesions. Both, vascular pathology as well as metabolic disturbances induced by toxins of activated macrophages and microglia may be responsible for such lesions in multiple sclerosis.
Lassmann
Hans
H
Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria. hans.lassman@univie.ac.at
D002490:Central Nervous System / Q000293:injuries / Q000473:pathology*; D003711:Demyelinating Diseases / Q000209:etiology; D004660:Encephalitis / Q000209:etiology / Q000473:pathology; D006801:Humans; D000860:Hypoxia / Q000209:etiology; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology / Q000473:pathology; D009103:Multiple Sclerosis / Q000145:classification / Q000473:pathology*; D009836:Oligodendroglia / Q000473:pathology