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

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 beta-amyloid (A beta 25 - 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 A beta or endothelin alone but was less effective in the more severe pathology of the combined A beta/endothelin model. Conclusions - Higher doses or more prolonged treatment with NSAIDs may be required for more effective neuroprotection in combined AD and stroke conditions.