%0 Journal Article
%T Brain gangliosides of a transgenic mouse model of Alzheimer's disease with deficiency in GD3-synthase: expression of elevated levels of a cholinergic-specific ganglioside, GT1a¦Á
%A Toshio Ariga
%A Yutaka Itokazu
%A Michael£¿P. McDonald
%A Yoshio Hirabayashi
%J ASN Neuro
%D 2013
%I 
%R 10.1042/an20130006
%X In order to examine the potential involvement of gangliosides in AD (Alzheimer's disease), we compared the ganglioside compositions of the brains of a double-transgenic (Tg) mouse model [APP (amyloid precursor protein)/PSEN1 (presenilin)] of AD and a triple mutant mouse model with an additional deletion of the GD3S (GD3-synthase) gene (APP/PSEN1/GD3S / ). These animals were chosen since it was previously reported that APP/PSEN1/GD3S /  triple-mutant mice performed as well as WT (wild-type) control and GD3S /  mice on a number of reference memory tasks. Cholinergic neuron-specific gangliosides, such as GT1a¦Á and GQ1b¦Á, were elevated in the brains of double-Tg mice (APP/PSEN1), as compared with those of WT mice. Remarkably, in the triple mutant mouse brains (APP/PSEN1/GD3S / ), the concentration of GT1a¦Á was elevated and as expected there was no expression of GQ1b¦Á. On the other hand, the level of c-series gangliosides, including GT3, was significantly reduced in the double-Tg mouse brain as compared with the WT. Thus, the disruption of the gene of a specific ganglioside-synthase, GD3S, altered the expression of cholinergic neuron-specific gangliosides. Our data thus suggest the intriguing possibility that the elevated cholinergic-specific ganglioside, GT1a¦Á, in the triple mutant mouse brains (APP/PSEN1/GD3S / ) may contribute to the memory retention in these mice.
%K Alzheimer¡¯s disease
%K amyloid ¦Â protein
%K Chol-1¦Á ganglioside
%K transgenic mouse
%U http://www.asnneuro.org/an/005/e113/an005e113.htm