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, GT1aα.
ASN Neuro
; 5(2): 141-8, 2013 May 30.
Article
em En
| MEDLINE
| ID: mdl-23565921
ABSTRACT
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 GT1aα and GQ1bα, 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 GT1aα was elevated and as expected there was no expression of GQ1bα. 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, GT1aα, in the triple mutant mouse brains (APP/PSEN1/GD3S(-/-)) may contribute to the memory retention in these mice.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Sialiltransferases
/
Encéfalo
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Regulação da Expressão Gênica
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Neurônios Colinérgicos
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Doença de Alzheimer
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Gangliosídeos
Tipo de estudo:
Etiology_studies
Limite:
Animals
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Humans
Idioma:
En
Revista:
ASN Neuro
Ano de publicação:
2013
Tipo de documento:
Article