P. Odetti et al., EARLY GLYCOXIDATION DAMAGE IN BRAINS FROM DOWNS-SYNDROME, Biochemical and biophysical research communications, 243(3), 1998, pp. 849-851
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.