This Article Full Text Full Text (PDF) All Versions of this Article: 36/8/1782    most recent 01.STR.0000173405.02425.d6v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Whitehead, S. Articles by Cechetto, D. F. Search for Related Content PubMed PubMed Citation Articles by Whitehead, S. Articles by Cechetto, D. F. Related Collections Animal models of human disease Acute Cerebral Infarction

(Stroke. 2005;36:1782.)
© 2005 American Heart Association, Inc.

Original Contributions

Interaction Between a Rat Model of Cerebral Ischemia and ß-Amyloid Toxicity

II. Effects of Triflusal

From the Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada.

Correspondence to David F. Cechetto, Department of Anatomy and Cell Biology, Medical Sciences Building, University of Western Ontario, London, ON, Canada N6A 5C1.

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 ß-amyloid (Aß25–35) 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 Aß or endothelin alone but was less effective in the more severe pathology of the combined Aß/endothelin model.

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

Key Words: amyloid • anti-inflammatory agents • astrocytes • cytokines • microglia

This article has been cited by other articles:

				S. N. Whitehead, G. Cheng, V. C. Hachinski, and D. F. Cechetto Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid Stroke, December 1, 2007; 38(12): 3245 - 3250. [Abstract] [Full Text] [PDF]