Journal
NEUROBIOLOGY OF DISEASE
Volume 38, Issue 3, Pages 482-491Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2010.01.019
Keywords
Alzheimer's disease; Transgenic mice; Triflusal; Amyloid; Neuroinflammation; Cytokines; Cognition; CREB; c-fos; BDNF
Categories
Funding
- FIS [PI041887]
- CIBERNED
- NIH [AG020570]
- Marato [072610]
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Inflammation has been associated with the two classic lesions in the Alzheimer's (AD) brain, amyloid deposits and neurofibrillary tangles. Recent data suggest that Triflusal, a compound with potent anti-inflammatory effects in the central nervous system in vivo, might delay the conversion from amnestic mild cognitive impairment to a fully established clinical picture of dementia. In the present study, we investigated the effect of Triflusal on brain A beta accumulation, neuroinflammation, axonal curvature and cognition in an AD transgenic mouse model (Tg2576). Triflusal treatment did not alter the total brain A beta accumulation but significantly reduced dense-cored plaque load and associated glial cell proliferation, proinflammatory cytokine levels and abnormal axonal curvature, and rescued cognitive deficits in Tg2576 mice. Behavioral benefit was found to involve increased expression of c-fos and BDNF, two of the genes regulated by CREB, as part of the signal transduction cascade underlying the molecular basis of long-term potentiation. These results add preclinical evidence of a potentially beneficial effect of Triflusal in AD. (C) 2010 Elsevier Inc. All rights reserved.
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