Journal
BRAIN RESEARCH
Volume 1368, Issue -, Pages 239-247Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2010.10.053
Keywords
Alzheimer's disease; Tumor necrosis factor-alpha; Amyloid plaque; Tau phosphorylation; CD11c-positive dendritic-like cell
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Funding
- National Natural Science Foundation of China [30700248]
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inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). Overexpression of tumor necrosis factor-alpha (TNF-alpha) occurs in the AD brain. Recent clinical studies have shown that the anti-TNF-alpha therapy improves cognition function of AD patients rapidly. However, the underlying mechanism remains elusive. The present study investigates the effects of intracerebroventricular injection of the monoclonal TNF-alpha antibody, Infliximab, on the pathological features of AD in the APP/PS1 double transgenic mice. We found that infliximab administration reduced the levels of TNF-alpha, amyloid plaques, and tau phosphorylation as early as three days after daily injection of 150 mu g Infliximab for three days. The number of CD11c-positive dendritic-like cells and the expression of CD11c were found to be increased concurrently after Infliximab injection. These data suggested that the CD11c-positive dendritic-like cells might contribute to the Infliximab-induced reduction of AD-like pathology. Furthermore, our results support the use of anti-TNF-alpha for the treatment of AD. (C) 2010 Elsevier B.V. All rights reserved.
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