期刊
JOURNAL OF NEUROENDOCRINOLOGY
卷 25, 期 4, 页码 350-356出版社
WILEY
DOI: 10.1111/jne.12006
关键词
spironolactone; JNK inhibition; Tau; hippocampus; cognition; caspase; stress
资金
- FIS [10/01748]
- CAN
- Ministerio de Educacion y Ciencia (Spain)
It is becoming evident that chronic exposure to glucocorticoids might not only result in insulin resistance or cognitive deficits, but also is considered as a risk factor for pathologies such as depression or Alzheimer's disease. In the present study, in vivo experiments using a non-invasive method of chronic administration of corticosterone in drinking water demonstrated that chronic corticosterone administration led to cognitive impairment in the novel object recognition test and insulin resistance, as shown by significant increases in plasma insulin levels and the homeostatic model assessment index, and decreased insulin receptor phosphorylation. Corticosterone treatment induced an increased expression of stress-activated c-Jun N-terminal kinase (JNK) in the hippocampus, accompanied by decreases in glycogen synthase kinase 3, increases in pTau levels and increased neuronal cell death (caspase-3 activity). All these effects were reversed by the administration of a JNK1 inhibitor or by the mineralocorticoid receptor antagonist spironolactone. It is suggested that the mineralocorticoid receptors and JNK-mediated pathways are involved in the interaction of glucocorticoid-insulin resistance and the development of relevant cellular processes for Alzheimers disease
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据