[S100B: pathogenetic and pathophysiologic significance in neurology].

S100B is a multifunctional member of the S100-calmodulin-troponin superfamily of proteins and can modulate the activity of other intracellular proteins following binding of calcium. S100B has been shown to exhibit regulatory effects on cell growth and differentiation as well as on cell shape and energy metabolism. S100B has neurotrophic properties and stimulates glial cell proliferation in vitro and in vivo. Overexpression of S100B has been proposed as a pathogenetic factor in plaque formation in patients with Alzheimerís disease and Down syndrome. Furthermore, S100B-specific T-lymphocytes have been shown to be encephalitogenic in the animal model of experimental autoimmune panencephalitis (EAP). Phenotypically and functionally similar S100B-specific T-cells can also be recovered from the peripheral blood of humans making S100B a potential candidate autoantigen in multiple sclerosis. Here the basic biochemical, molecular and functional properties of S100B are reviewed with special regard to the potential pathogenetic role of S100B in Alzheimerís disease, Down syndrome and multiple sclerosis.