Gangliosides in the brain in adult Down's syndrome and Alzheimer's disease

• Published in: Molecular and chemical neuropathology 1989-12, Vol.11 (3), p.143-156
• Main Authors: BROOKSBANK, B. W. L, MCGOVERN, J
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - metabolism; Biological and medical sciences; Brain Chemistry - physiology; Cerebellum - chemistry; Choline O-Acetyltransferase - metabolism; Corpus Callosum - chemistry; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Down Syndrome - metabolism; Frontal Lobe - chemistry; Gangliosides - analysis; Humans; Medical sciences; Middle Aged; Neurology; Sialic Acids - analysis
• ISSN: 1044-7393; 2168-8729
• DOI: 10.1007/BF03160048

Quantitative analysis of total gangliosides and of ganglioside composition by HPTLC has been carried out on the gray matter of frontal cerebral cortex of six brains from Down's syndrome (DS) adults, six age-matched controls, six Alzheimer's disease (AD) adults, and six controls matched for age with the AD brains, as well as on three DS and six control cerebellum specimens. In addition, the analyses were carried out on specimens of corpus callosum of five adult DS and five control brains. No abnormalities were found in the gangliosides of DS corpus callosum. In DS frontal cortex, the concentration of total gangliosides was reduced, and there was a decrease in the fraction of GT1b and GD1b, and an increase in those of GT1a, GD3, GM1 and GM2; the ratio of total b-series to a-series gangliosides was decreased. Very similar abnormalities were found in the gangliosides of DS cerebellum. In AD frontal cortex, by contrast, the total gangliosides and their composition were normal by comparison with age-matched controls, with the minor exception of reductions in the fractions of GQ1b and GT1L. It is concluded that abnormalities in gangliosides exist in the brain in DS that are unrelated to AD-type pathology and may reflect developmental disturbances.