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- W2091492562 abstract "Several studies have implicated insulin and insulin-like growth factor-1 (IGF-1) Signaling (IIS) as being involved in the pathogenesis of AD. To investigate the role of neuronal IIS in AD we generated neuron-specific IGF-1R (nIGF-1R-/-) and Insulin receptor (nIR-/-) deficient mice. These mice were crossed with Tg2576 mice, a well established AD model. We generated nIGF-1R-/- and nIR-/- mice using the cre-loxP-system under the control of the neuron-specific synapsin-1 promoter and crossed them into the Tg2576 background. The offsprings of these mice (WT, Tg2576, nIGF-1R-/-, Tg2576/nIGF-1R-/-, nIR-/-, Tg2576/nIR-/-) were analysed. As described previously Kaplan-Meier-analysis revealed a 60% mortality of Tg2576 mice after 60 weeks of observation. In contrast only 35% of Tg2576/nIGF-1R-/- died within the same time. Thus, Tg2576/nIGF-1R-/- were protected against premature mortality of Tg2576 mice (p ≤ 0.02; Tg2576 vs. Tg2576/nIGF-1R-/-). However, neuronal IR deletion had no influence on Tg2576 mortality. Western blot analysis of isolated hippocampi displayed a 40% reduced IGF-1R expression in nIGF-1R-/- and Tg2576/nIGF-1R-/- compared to WT and Tg2576 animals, whereas other brain regions e.g. cortex or cerebellum did not show significant IGF-1R alteration. Furthermore, hippocampi of 28 and 60 weeks old Tg2576/nIGF-1R-/- animals showed a 50% reduced Aβ1-40 and Aβ1-42 accumulation compared to Tg2576. Additionally, APP α/βC-terminal fragments were reduced in hippocampi of Tg2576/nIGF-1R-/- compared Tg2576 mice, indicating modified APP processing. Taken together our results demonstrate that decreased neuronal IGF-1R signaling leads to reduced Aβ accumulation and protects against premature death of Tg2567 mice." @default.
- W2091492562 created "2016-06-24" @default.
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- W2091492562 date "2009-07-01" @default.
- W2091492562 modified "2023-09-27" @default.
- W2091492562 title "O1-03-08: Neuronal IGF-1 resistance protects against premature death and reduces β -Amyloid accumulation in Tg2576 mice" @default.
- W2091492562 doi "https://doi.org/10.1016/j.jalz.2009.05.212" @default.
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