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  • Title: Altered expression of Abeta metabolism-associated molecules from D-galactose/AlCl(3) induced mouse brain.
    Author: Luo Y, Niu F, Sun Z, Cao W, Zhang X, Guan D, Lv Z, Zhang B, Xu Y.
    Journal: Mech Ageing Dev; 2009 Apr; 130(4):248-52. PubMed ID: 19150622.
    Abstract:
    Cerebral deposition of amyloid-beta peptide (Abeta) is a critical feature of Alzheimer's disease (AD). Either aluminium trichloride (Al) or D-galactose (D-gal) induces Abeta overproduction in rat or mouse brain and has been used to produce models of aging and AD. Here it is shown that mice treated with Al plus D-gal represent a good model of AD with altered expression of Abeta metabolism-associated molecules. The work shows that Al/D-gal causes memory impairment and high Abeta levels in the cortex (Co) and hippocampus (Hi). Then, we found that beta-site APP cleavage enzyme 1 (BACE1) was increased in mouse Co and Hi. Al or Al plus D-gal suppressed mRNA of the low-density lipoprotein receptor-related protein 1(LRP1). D-gal also decreased the LRP expression in Hi, but not in Co. However, Al/D-gal did not affect the receptor for advanced glycation end products (RAGE) expression in mouse brains. Furthermore, Al/D-gal reduced the expression of neprilysin (NEP), but not the insulin degrading enzyme (IDE). This study indicates that Al/D-gal affects the expression of Abeta metabolism-associated molecules that are responsible for Abeta deposition during AD, suggesting that this mouse model can be a useful model for studying the mechanisms and biomarkers of AD and for drug screening.
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