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Treatment at the Institute of Neurological Recovery in Boca Raton, Florida, in April, 2017.
Welcome to the INR Blog!
This Blog is still in development. The aim of this blog is to add further scientific information to the content of the INR website as soon as it becomes available. If possible in the future postings and comments from website visitors will be enabled. Thank you for your interest.
Edward Tobinick MD
Recent published research results:
Anti-TNF-alpha reduces amyloid plaques and tau phosphorylation and induces CD11c-positive dendritic-like cell in the APP/PS1 transgenic mouse brains. Shi JQ, Shen W, Chen J, Wang BR, Zhong LL, Zhu YW, Zhu HQ, Zhang QQ, Zhang YD, Xu J. Brain Res. 2010 Oct 21.
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 150micrograms of 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. Further, our results support the use of anti-TNF-alpha for the treatment of AD. Continue reading