Myelin constituents of human central nervous system.

TLDR: Recently, accounts have been presented of the complete quantitativc distribution of membrane constituents in grey matter, white matter, and in myelin and other subcellular particulate fractions of the central nervous system (CNS) (survey by Mokrasch 1969, Rouser & Yarriainoto 1969, Clausen 1969).

Abstract: Recently, accounts have been presented of the complete quantitativc distribution of membrane constituents in grey matter, white matter, and in myelin and other subcellular particulate fractions of the central nervous system (CNS) (survey by Mokrasch 1969, Rouser & Yarriainoto 1969, Clausen 1969). Data from these studies have made possible a morc detailed elucidation of the changes of CNS under pathological conditions. e.g. multiple sclerosis (MS) . Although it has been shown that chemical changes related to the plaque formation characteristic of hlS involve disappearance of myelin constituents, deposits of cholesterol esters (survey by McAlpine, Lumsden & Acheson 1965) and increase in enzymic activities of zones surrounding the plaques (Friede 1966), the pathogenesis of MS is still obscure. In order to avoid the difficulties of exploring pathogenesis on the basis of studies of plaques with a population of cells differing from that of the original tissue (Greenfield et al. 1960), studies of MS in recent years have been concerned with the so-called normal white matter from MS patients. Such studies, based upon a rather small number of autopsy specimens, have revealed inconsistent changes in the composition of myelin, or of whole white matter. In a study of myelin from 3 cases of MS, Cumings & Goodwin ( 1968) demonstrated a decrease in the cerebroside/sulfatide ratio, and Gerstl et al. (1965) showed that M S myelin from 2 M S patients contained less cerebroside than normal myelin. The slight increase in fatty acid saturation found in the so-called “normal” MS white matter and myelin from MS patients (Cumings, Shortman & Skrbic 1966, Gerstl et al. 1965, Thompson 1966) may be related either to dietary, infectious or anoxic factors (vide infra) or to changes in the polar lipid and cholesterol composition, since the fatty acid profiles of phosphoand glycolipids differ (survey by Clausen 1969).