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- Author: Hettich Moritz M
- Publisher: Sudwestdeutscher Verlag Fur Hochschulschriften AG
- Year: 2011
- Pages: 116
- ISBN-10: 3838128788
- ISBN-13: 9783838128788
- Format: 15.2 x 22.9 x 0.7 cm, softcover
- Language: English
- SAVE -10% with code: EXTRA
Role of neuronal IGF-1R signaling in Alzheimer's disease (e-book) (used book) | bookbook.eu
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Brains from patients with AD reveal a markedly down regulaton of IGF-1R expression and these changes progress with severity of neurodegeneration. To investigate the role of neuronal IGF-1R signaling in AD a neuron-specific IGF-1R deficient mice were generated and were crossed with mice expressing mutated human APP which was found in a Swedish family with early-onset AD. The offsprings of these mice were analysed. Kaplan-Meier-analysis after 60 weeks of observation revealed that nIGF-1R knockout mice were protected against premature mortality of AD mice and showed reduced Aβ accumulation. In addition Aβ plaque burden in animals with neuronal IGF-1R deletion was also reduced compared to AD animals. Taken together IGF-1R mediated signals influence APP processing leading to reduced Aβ accumulation and amyloid plaque burden. Thus, downregulation of IGF-1R observed in brain of patients suffering from Alzheimer's disease is most likely a compensatory phenomenon.
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- Author: Hettich Moritz M
- Publisher: Sudwestdeutscher Verlag Fur Hochschulschriften AG
- Year: 2011
- Pages: 116
- ISBN-10: 3838128788
- ISBN-13: 9783838128788
- Format: 15.2 x 22.9 x 0.7 cm, softcover
- Language: English English
Brains from patients with AD reveal a markedly down regulaton of IGF-1R expression and these changes progress with severity of neurodegeneration. To investigate the role of neuronal IGF-1R signaling in AD a neuron-specific IGF-1R deficient mice were generated and were crossed with mice expressing mutated human APP which was found in a Swedish family with early-onset AD. The offsprings of these mice were analysed. Kaplan-Meier-analysis after 60 weeks of observation revealed that nIGF-1R knockout mice were protected against premature mortality of AD mice and showed reduced Aβ accumulation. In addition Aβ plaque burden in animals with neuronal IGF-1R deletion was also reduced compared to AD animals. Taken together IGF-1R mediated signals influence APP processing leading to reduced Aβ accumulation and amyloid plaque burden. Thus, downregulation of IGF-1R observed in brain of patients suffering from Alzheimer's disease is most likely a compensatory phenomenon.
Reviews