Interaction between a rat model of cerebral ischemia and β-amyloid toxicity: II. Effects of triflusal

Abstract

Background and Purpose - Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Our rat model demonstrates that this interaction may be mediated through inflammatory cells and pathways. Thus, anti-inflammatory agents such as Triflusal, a nonsteroidal anti-inflammatory agent (NSAID), may provide neuroprotection for susceptible neurons in AD and cerebral ischemia. Methods - AD was modeled by cerebroventricular injections of β-amyloid (Aβ25-35) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined by immunohistochemical analysis. Behavioral tasks were assessed with the Montoya staircase test. Results - Triflusal reduced pathologic and inflammatory markers and functional deficits in rats receiving Aβ or endothelin alone but was less effective in the more severe pathology of the combined Aβ/endothelin model. Conclusions - Higher doses or more prolonged treatment with NSAIDs may be required for more effective neuroprotection in combined AD and stroke conditions. © 2005 American Heart Association, Inc.