| First Author | Hillmann A | Year | 2012 |
| Journal | Neurobiol Aging | Volume | 33 |
| Issue | 4 | Pages | 833.e39-50 |
| PubMed ID | 21943956 | Mgi Jnum | J:188189 |
| Mgi Id | MGI:5439676 | Doi | 10.1016/j.neurobiolaging.2011.08.006 |
| Citation | Hillmann A, et al. (2012) No improvement after chronic ibuprofen treatment in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 33(4):833.e39-50 |
| abstractText | Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) that has been reported to reduce the risk of developing Alzheimer's disease (AD). Its preventive effects in AD are likely pleiotropic as ibuprofen displays both anti-inflammatory activity by inhibition of cyclooxygenases and anti-amyloidogenic activity by modulation of gamma-secretase. In order to study the anti-inflammatory properties of ibuprofen independent of its anti-amyloidogenic activity, we performed a long-term treatment study with ibuprofen in 5XFAD mice expressing a presenilin-1 mutation that renders this AD model resistant to gamma-secretase modulation. As expected, ibuprofen treatment for 3 months resulted in a reduction of the inflammatory reaction in the 5XFAD mouse model. Importantly, an unchanged amyloid beta (Abeta) plaque load, an increase in soluble Abeta42 levels, and an aggravation of some behavioral parameters were noted, raising the question whether suppression of inflammation by nonsteroidal anti-inflammatory drug is beneficial in AD. |
