| First Author | Perez Nievas BG | Year | 2011 |
| Journal | J Neurochem | Volume | 116 |
| Issue | 1 | Pages | 43-52 |
| PubMed ID | 21044080 | Mgi Jnum | J:167060 |
| Mgi Id | MGI:4867113 | Doi | 10.1111/j.1471-4159.2010.07083.x |
| Citation | Perez Nievas BG, et al. (2011) Restraint stress increases neuroinflammation independently of amyloid beta levels in amyloid precursor protein/PS1 transgenic mice. J Neurochem 116(1):43-52 |
| abstractText | Both hypercortisolemia and hippocampal damage are features found in patients diagnosed of Alzheimer's disease (AD) and epidemiological evidence supports a role for stress as a risk factor for AD. It is known that immobilization stress is followed by accumulation of oxidative/nitrosative mediators in brain after the release of proinflammatory cytokines, nuclear factor kappa B activation, nitric oxide synthase-2 and cyclooxygenase-2 expression. Long-term exposure to elevated corticosteroid levels is known to affect the hippocampus which plays a central role in the regulation of the hypothalamic-pituitary-adrenal axis. We therefore studied the effect of chronic immobilization stress on amyloid precursor protein/PS1 mice. Stress exposure increased AD-induced neuroinflammation characterized by astrogliosis, increased inflammatory gene transcription and lipid peroxidation. Importantly, immobilization stress did not increase the soluble or insoluble amyloid beta levels suggesting that increased cortisol levels lower the threshold for a neuroinflammatory response, independently from amyloid beta. Since inflammation may act as a factor that contributes disease progression, the stress-inflammation relation described here may be relevant to understand the initial mechanisms in underlying the risk enhancing action of stress on AD. |
