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• W2108570372 abstract "Studies have shown that acute injuries, i.e. brain trauma and stroke, can cause a rapid production of TNFa in glial cells and neurons while endogenous TNFα may modulate responses chronic brain disorders. As most of cytokines, TNFα, is expressed at very low levels in the healthy brain. The elevation of cytokines caused by disease-related neuroinflammation could be detected much earlier than neuronal death. The biological effect of TNFα is mediated via its receptors (TNFRI and TNFRII). Our recent studies showed that changes in TNFα receptors expression level might be responsible for the early inflammatory event of Alzheimer's disease (AD) in human (Cheng et al., 2010). Our studies also showed that TNFα induced elevation of BACE1 activity is mediated through the TNFRI/NF-kB signal cascade, which is required for Aß production (He et al., 2007). In concert with the human studies, depletion of the TNFRI gene in APP23 transgenic mice (APP23/TNFRI-/-) inhibits Aß generation and diminishes Aß plaque formation in the brain. These findings suggest that TNFRI might be a novel therapeutic target for AD since it not only contributes to neurodegeneration but also involves in APP processing and Aß plaque formation. Clinically, Tobinick (2007) has reported a significant beneficial effect of Entanacept (TNFα inhibitor) anecdotally to bypass brain blood barrier (BBB) in AD patient. Our preliminary data showed that Thalidomide, a small molecule TNFα inhibitor and can pass BBB, directly modulates TNFα mRNA expression and TNFα production. Here, we test this notion by using Thalidomide on Alzheimer's transgenic mice and examine whether Thalidomide could reduce Alzheimer's-like pathology. AD transgenic mice and wildtype mice received various dosages of Thalidomide treatment over time. Tissues were harvested for evaluation of several candidate genes associated with beta amyloid generation and degradation in AD. We discovered that numbers of amyloid plaque are significantly decreased in AD transgenic mice after thalidomide treatment compared to the mice treated with vehicle at the same age. Moreover, three key genes that involved in beta amyloid production are significantly altered after thalidomide treatments. More detailed data and discussion will be presented during the ICAD meeting. As a proof of this concept, Thalidomide, as a TNFα inhibitor and an existing drug for arthritis, may be a logical drug candidate for AD treatment due to its special property in regulation of APP processing and other genes in AD pathology." @default.
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• W2108570372 date "2011-07-01" @default.
• W2108570372 modified "2023-09-27" @default.
• W2108570372 title "P2-501: Novel roles of Thalidomide in Alzheimer's disease" @default.
• W2108570372 doi "https://doi.org/10.1016/j.jalz.2011.05.1372" @default.
• W2108570372 hasPublicationYear "2011" @default.
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