EARLY GLYCOXIDATION DAMAGE IN BRAINS FROM DOWNS-SYNDROME

Citation
P. Odetti et al., EARLY GLYCOXIDATION DAMAGE IN BRAINS FROM DOWNS-SYNDROME, Biochemical and biophysical research communications, 243(3), 1998, pp. 849-851
Citations number
17
Categorie Soggetti
Biology,Biophysics
ISSN journal
0006291X
Volume
243
Issue
3
Year of publication
1998
Pages
849 - 851
Database
ISI
SICI code
0006-291X(1998)243:3<849:EGDIBF>2.0.ZU;2-L
Abstract
In Down's syndrome, the presence of three copies of chromosome 21 is a ssociated with premature aging and progressive mental retardation shar ing the pathological features of Alzheimer disease, Early cortical dys genesis and late neuronal degeneration are probably caused by an overp roduction of amyloid beta-peptide, followed by an increased cellular o xidation. Interestingly, chromosome 21 codes for superoxide-dismutase and amyloid beta precursor resulting, in Down's syndrome, in an overfl ow of these gene products and metabolites. We studied Down's fetal bra in cortex to evaluate the presence and amount of lipid and protein oxi dation markers; moreover, we quantified two forms of glycation end pro ducts that are known to be involved in the process of cellular oxidati on. All these parameters are significantly increased in Down's fetal b rains in comparison to controls, providing the evidence that accelerat ed brain glycoxidation occurs very early in the life of Down's syndrom e subjects. (C) 1998 Academic Press.