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Stroke. 2005 Aug;36(8):1782-9. Epub 2005 Jul 21.

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

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  • 1Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada.

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 beta-amyloid (Abeta25-35) 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 Abeta or endothelin alone but was less effective in the more severe pathology of the combined Abeta/endothelin model.

CONCLUSIONS:

Higher doses or more prolonged treatment with NSAIDs may be required for more effective neuroprotection in combined AD and stroke conditions.

PMID:
16040593
[PubMed - indexed for MEDLINE]
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