SOD-1 inhibits FAS expression in cortex of APP transgenic mice.
Peptides derived from proteolytic processing of the amyloid precursor protein (APP) are important for the pathogenesis of Alzheimer's disease (AD). In the present study, we found that transgenic mice overexpressing wild-type human APP gene (hAPP/+) displayed a much higher expression of FAS, one of the death receptor subfamily. This FAS overexpression was significantly reduced in the cortex of mice overexpressing both wild-type hAPP gene and wild-type human superoxide dismutase-1 gene (hSOD-1). Moreover hSOD-1 transgenic expression was associated with an increase of Glial fibrillary acidic protein (GFAP) production. This study indicates that SOD-1 overexpression can inhibit FAS expression, which may be beneficial in AD.
Chen
Z
Z
Division of Experimental Geriatrics, Department of Neurotec, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
Duan
R-S
RS
Lepécheur
M
M
Paly
E
E
London
J
J
Zhu
J
J
D000544:Alzheimer Disease / Q000503:physiopathology; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis*; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D006801:Humans; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D013482:Superoxide Dismutase / Q000378:metabolism*; D000072105:Superoxide Dismutase-1; D019014:fas Receptor / Q000096:biosynthesis*
D016564:Amyloid beta-Protein Precursor; D005904:Glial Fibrillary Acidic Protein; C000606290:SOD1 protein, human; D019014:fas Receptor; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1