Moritz Hettich (5 results)

Condition: New.

Taschenbuch. Condition: Neu. Role of neuronal IGF-1R signaling in Alzheimer's disease | Involvement in development and progression | Moritz M. Hettich | Taschenbuch | 116 S. | Englisch | 2015 | Südwestdeutscher Verlag für Hochschulschriften | EAN 9783838128788 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu.

Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -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 Abeta accumulation. In addition Abeta 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 Abeta 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. 116 pp. Englisch.

Taschenbuch. Condition: Neu. This item is printed on demand - Print on Demand Titel. Neuware -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 A¿ accumulation. In addition A¿ 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 A¿ 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.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 116 pp. Englisch.

Taschenbuch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - 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 Abeta accumulation. In addition Abeta 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 Abeta 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.