Ganglioside content and composition were studied in whole brains from 9 neurologically normal male individuals ranging from 25 to 85 years in age. The content of ganglioside-bound sialic acid decreased from 1,070 to 380 μg/g fresh tissue at 85 years. Ten individual ganglioside fractions were identified on high-performance thin-layer chromatography, seven of which were quantified. With age, ganglioside composition shifted to a more polar pattern due to an increase in the relative concentration of the more polar fractions GQ1b, GT1b and GD1b and a decrease in GD1 a and GM1. Except for GQ1b, the absolute concentration of all gangliosides decreased with age. All changes were more pronounced in younger ages. Results are discussed in relation to structural changes occurring in the aging brain, and the involvement of gangliosides is suggested.

Developmental profiles of 11 gangliosides, concentration of lipid- and glycoprotein-bound sialic acid, and activity of AChE of the rat and mouse cerebral cortex were followed from the 7 day of gestation to the 21 postnatal day.There are three main changes in ganglioside concentration, which are similar in both species. The first occurs from gestation day 10 until birth: parallel to decreased proliferation, cell migration, and neuroblast differentiation, G and G in mouse cortex and G in the rat's decreases in favor of G, G, and G.The second occurs from birth until the first postnatal week: Parallel to increased growth and arborization of dendrites and axons as well as synaptogenesis in rats and mice, there is a two-fold rise of G, whereas G and G remain on a nearly constant level. Concomitantly, G and G decreases. The third period of ganglioside changes starts in the second postnatal week, parallel to onset of myelination, and is characterized by an increase of G in parallel with a decrease of the polysialogangliosides G and G.

Experimental spinal cord trauma was produced in 3-month-old SS-1 miniature pigs by dropping a 25 g weight from a height of 20 cm upon the exposed spinal cord. The histological lesion consisted of edema and hemorrhage. Phospholipid concentration and composition, cholesterol concentration and phospholipid fatty acid composition were determined in whole spinal cord 3 hours after injury, and in spinal cord myelin 5 hours after injury. Three hours after injury phospholipid and cholesterol concentration were decreased by about 14% in the whole spinal cord. Trauma had no effect on the phospholipid composition of whole spinal cord and myelin. Fatty acid composition of myelin also did not change after injury, and changed very slightly in the whole spinal cord. It is concluded that edema following spinal cord trauma is much more extensive than previously assumed. Furthermore, peroxidation of membrane lipid fatty acids does not appear to be a significant factor in spinal cord pathology 3 hours after injury.

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