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• W2016666073 abstract "The insulin-degrading enzyme (IDE) is a zinc metallo-endopeptidase that degrades monomeric beta-amyloid peptides (Abeta). IDE deficiency has previously been shown to lead to accumulation of murine cerebral Abeta40 and Abeta42 in 3 and 6 month old IDE deficient mice (IDE KO). However, lower brain Abeta levels and hippocampal Abeta load were unexpectedly found in 13 month-old IDE KO/J9 mice when compared to J9 age-matched controls. Altered brain levels of amyloid precursor protein (APP) holoprotein or APP C-terminal fragments do not account for this difference. Given our data that younger IDE KO/J9 mice (3 month-old) show elevated levels of soluble Abeta40 and Abeta42 in the brain, we hypothesized that IDE deficiency enhances local Abeta clearance mechanisms triggered by the age-dependent accumulation of Abeta fibrils and/or oligomeric intermediates in the brain. To determine whether the astrocytic or microglial inflammatory response contributes to enhanced Abeta clearance in IDE KO/J9 mice, GFAP and CD45 immunohistochemical staining was performed in aged mice (13 and/or 16 months old). MCID Elite Imaging software was used for densitometric quantitation of load in the hippocampus. Densitometric quantitation of GFAP in IDE KO/J9 and J9 hippocampi revealed a trend towards increased astrocytic activation in the J9/IDE KO mice (% hippocampal area 1.73 and 1.25 at 13 months; 1.30 and 1.16 at 16 months; respectively). In contrast, our preliminary data on CD45 microglia show a decreased microglial response in 16 month-old IDE KO/J9 mice. Abeta immunohistochemical staining of 16 month-old IDE KO/J9 and J9 brains confirmed our previous findings that hippocampal Abeta load in IDE KO/J9 mice is lower than in J9 controls (57%, p<0.05, n=6 and 7). No differences in the levels of the following Abeta degrading enzymes: neprilysin, cathepsin B and cathepsin D, were observed in 13 month-old IDE KO/J9 and J9 brain extracts. Our results indicate that IDE deficiency slows Abeta deposition in J9 APP transgenic mice and that this may be due to enhanced Abeta clearance by activated astrocytes. The possibility that IDE deficient astrocytes contribute directly to enhanced Abeta clearance is currently being studied." @default.
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• W2016666073 date "2009-07-01" @default.
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• W2016666073 title "P1-021: Activated astrocytes may contribute to lower levels of soluble and aggregated β-amyloid in insulin-degrading enzyme knockout/APP transgenic mice" @default.
• W2016666073 doi "https://doi.org/10.1016/j.jalz.2009.04.024" @default.
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