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- Autorius: Hettich Moritz M
- Leidėjas: Sudwestdeutscher Verlag Fur Hochschulschriften AG
- Metai: 2011
- Puslapiai: 116
- ISBN-10: 3838128788
- ISBN-13: 9783838128788
- Formatas: 15.2 x 22.9 x 0.7 cm, minkšti viršeliai
- Kalba: Anglų
Role of neuronal IGF-1R signaling in Alzheimer's disease (el. knyga) (skaityta knyga) | knygos.lt
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Aprašymas
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.
- Autorius: Hettich Moritz M
- Leidėjas: Sudwestdeutscher Verlag Fur Hochschulschriften AG
- Metai: 2011
- Puslapiai: 116
- ISBN-10: 3838128788
- ISBN-13: 9783838128788
- Formatas: 15.2 x 22.9 x 0.7 cm, minkšti viršeliai
- Kalba: Anglų
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.
Atsiliepimai