کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4326225 | 1614071 | 2011 | 9 صفحه PDF | دانلود رایگان |

Inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). Overexpression of tumor necrosis factor-α (TNF-α) occurs in the AD brain. Recent clinical studies have shown that the anti-TNF-α 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-α 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-α, amyloid plaques, and tau phosphorylation as early as three days after daily injection of 150 μg 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-α for the treatment of AD.
Research Highlights
► Intracerebroventricular administration of Infliximab, which is anti-TNF-α drug, decreases TNF-α in APP/PS1 transgenic mice.
► Infliximab decreases amyloid plaques and tau phosphorylation in APP/PS1 transgenic mice.
► The increase of local CD11c-positive dendritic-like cells in brain may be a possible mechanism.
Journal: Brain Research - Volume 1368, 12 January 2011, Pages 239–247