on July 21, 2005
Published online before print July 21, 2005, doi: 10.1161/01.STR.0000173405.02425.d6
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Submitted on April 22, 2005
From the Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada.
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 Results--Triflusal reduced pathologic and inflammatory markers and functional deficits in rats receiving A Conclusions--Higher doses or more prolonged treatment with NSAIDs may be required for more effective neuroprotection in combined AD and stroke conditions.
Accepted on May 2, 2005
Interaction Between a Rat Model of Cerebral Ischemia and
Shawn Whitehead BSc; 
-Amyloid Toxicity. II. Effects of Triflusal
-amyloid (A25-35) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined by immunohistochemical analysis. Behavioral tasks were assessed with the Montoya staircase test. or endothelin alone but was less effective in the more severe pathology of the combined A/endothelin model.
Key words: amyloid • anti-inflammatory agents • astrocytes • cytokines • microglia
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  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]
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