CIDeRplusGeneral Information:
| Id: | 6,481 (click here to show other Interactions for entry) |
| Diseases: |
Alzheimer disease
- [OMIM]
|
| Mammalia | |
| review | |
| Reference: | Folch J et al.(2015) The role of leptin in the sporadic form of Alzheimers disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin Life Sci. 140: 19-28 [PMID: 25998028] |
Interaction Information:
| Comment | It has been shown that both the accumulation of Abeta and apoE4 genotype result in a transient enhancement of Lep signalling that might lead to Lep resistance over time. The mechanisms by which Abeta and apoE4 affect LepR expression are unknown. |
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Formal Description Interaction-ID: 62475 |
gene/protein mutant increases_activity of |
| Comment | Abeta and apoE4 genotype have been shown to cause inflammation, and LepR upregulation has been demonstrated in response to proinflammatory stimuli, such as treatments with LPS and TNFalpha. Transgenic animal models overexpressing human forms of Abeta or human apoE4, showed enhanced inflammatory reactions in the brain, including TNFalpha generation and gliosis. Thus, it may be speculated that the initial up-regulation of LepR could result from the pro-inflammatory effects of Abeta or apoE4. |
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Formal Description Interaction-ID: 62483 |
|
| Comment | Abeta and apoE4 genotype have been shown to cause inflammation, and LepR upregulation has been demonstrated in response to proinflammatory stimuli, such as treatments with LPS and TNFalpha. Transgenic animal models overexpressing human forms of Abeta or human apoE4, showed enhanced inflammatory reactions in the brain, including TNFalpha generation and gliosis. Thus, it may be speculated that the initial up-regulation of LepR could result from the pro-inflammatory effects of Abeta or apoE4. |
|
Formal Description Interaction-ID: 62516 |
gene/protein mutant increases_activity of phenotype |