CIDeRplusGeneral Information:
| Id: | 397 |
| Diseases: |
Alzheimer disease
- [OMIM]
|
| Mus musculus | |
| brain/neuron-specific insulin receptor knockout (NIRKO) mouse | |
| article | |
| Reference: | Schubert M et al.(2004) Role for neuronal insulin resistance in neurodegenerative diseases Proc. Natl. Acad. Sci. U.S.A. 101: 3100-3105 [PMID: 14981233] |
Interaction Information:
| Comment | Abolishing neuronal insulin signaling in NIRKO mice leads to major alterations in Akt and GSK3B phosphorylation and hyperphosphorylation of Tau protein at sites associated with neurodegenerative diseases. Altered insulin signaling in the brain leads to one of the hallmarks of Alzheimer's disease. |
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Formal Description Interaction-ID: 1698 |
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| Comment | Abolishing neuronal insulin signaling in NIRKO mice leads to major alterations in Akt and GSK3B phosphorylation and hyperphosphorylation of Tau protein at sites associated with neurodegenerative diseases. Altered insulin signaling in the brain leads to one of the hallmarks of Alzheimer's disease. |
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Formal Description Interaction-ID: 1701 |
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| Comment | NIRKO mice represent a unique model in which to study the consequences of isolated CNS-specific disruption of IR signaling on the biochemistry and function of the brain. The reduced phosphorylation of Akt and GSK3B in brains of NIRKO mice, in the presence of otherwise intact neurotrophic signaling, demonstrates directly the relative contribution and importance of IR signaling for the activation of this pathway in the CNS. |
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Formal Description Interaction-ID: 1705 |
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| Drugbank entries | Show/Hide entries for AKT1 |
| Comment | NIRKO mice represent a unique model in which to study the consequences of isolated CNS-specific disruption of IR signaling on the biochemistry and function of the brain. The reduced phosphorylation of Akt and GSK3B in brains of NIRKO mice, in the presence of otherwise intact neurotrophic signaling, demonstrates directly the relative contribution and importance of IR signaling for the activation of this pathway in the CNS. |
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Formal Description Interaction-ID: 1706 |
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| Drugbank entries | Show/Hide entries for GSK3B |
| Comment | Protein extracts from brains of NIRKO mice display a 3.5-fold increase in site-specific Tau hyperphosphorylation at Thr-231 but not at Ser-202. Phosphorylation of Tau at Thr-231 in humans has been correlated with cognitive decline and suggested as a biomarker for Alzheimer's disease. |
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Formal Description Interaction-ID: 1707 |
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| Comment | Protein extracts from brains of NIRKO mice display a 3.5-fold increase in site-specific Tau hyperphosphorylation at Thr-231 but not at Ser-202. Phosphorylation of Tau at Thr-231 in humans has been correlated with cognitive decline and suggested as a biomarker for Alzheimer's disease. |
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Formal Description Interaction-ID: 1708 |
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| Comment | Phosphorylation of Tau at Thr-231 in humans has been correlated with cognitive decline and suggested as a biomarker for Alzheimer's disease. |
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Formal Description Interaction-ID: 1709 |
protein modification MAPT-phosThr231 increases_activity of disease |
| Comment | NIRKO mice represent a unique model in which to study the consequences of isolated CNS-specific disruption of IR signaling on the biochemistry and function of the brain. The reduced phosphorylation of Akt and GSK3B in brains of NIRKO mice, in the presence of otherwise intact neurotrophic signaling, demonstrates directly the relative contribution and importance of IR signaling for the activation of this pathway in the CNS. |
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Formal Description Interaction-ID: 139769 |
organism model NIR KO mouse decreases_quantity of gene/protein NIR |
| Drugbank entries | Show/Hide entries for NIR |
| Comment | Protein extracts from brains of NIRKO mice display a 3.5-fold increase in site-specific Tau hyperphosphorylation at Thr-231 but not at Ser-202. Phosphorylation of Tau at Thr-231 in humans has been correlated with cognitive decline and suggested as a biomarker for Alzheimer's disease. |
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Formal Description Interaction-ID: 145057 |
organism model NIR KO mouse increases_quantity of protein modification MAPT-hyperphos |