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(Stroke. 2005;36:107.)
© 2005 American Heart Association, Inc.

Original Contributions

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

Inflammatory Responses

From the Department of Anatomy and Cell Biology (S.N.W., D.F.C.), and the Faculty of Medicine and Dentistry (V.C.H.), University of Western Ontario, London, Canada.

Correspondence to Dr David F. Cechetto, Department of Anatomy and Cell Biology, University of Western Ontario, London, Canada N6A 5C1. E-mail cechetto{at}uwo.ca

Background and Purpose— Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity.

Methods— AD was modeled by cerebroventricular injections of ß-amyloid (Aß[25–35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test.

Results— Aß injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites. Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and Aß(25–35). Aß(25–35) treatment decreased performance in the Montoya staircase behavioral test.

Conclusions— The enhanced inflammatory response with Aß toxicity and ischemia may mediate the inability to improve behavioral performance caused by the stroke. Anti-inflammatory treatment may ameliorate the pathological and behavioral deficits associated with the combination of AD and stroke.

Key Words: Alzheimer disease • astrocytes • ß-amyloid • cytokines • reactive microglia

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