Abstract
Background We previously showed the properties of interleukin-1b antagonist Anakinra on unmyelinated nerve fibers protection in a transgenic mouse model for human V30M transthyretin. In these studies, Anakinra decreased, among other markers, nerve levels of IL-1b, NFB and activated-caspase 3, associated with a decrease in TTRnon fibrillar deposition. In the present work, we compared the efficacy of other compounds under human therapeutical trials for Familial Amyloidotic Polyneuropathy (FAP) in the same animal model, having 5 months of age.
Highlights
We previously showed the properties of interleukin-1b antagonist Anakinra on unmyelinated nerve fibers protection in a transgenic mouse model for human V30M transthyretin
Other V30M mice group was treated with Tafamidis meglumine with 3 subcutaneous injections weekly, over 6 weeks
Efficiency of Anakinra as a neuroprotective molecule was corroborated in sciatic nerve analyses of NF-B, FAS death receptor and IL-1b in animals treated with a combination of Anakinra and siRNA, since these markers were found downregulated in animals receiving this combined therapy
Summary
We previously showed the properties of interleukin-1b antagonist Anakinra on unmyelinated nerve fibers protection in a transgenic mouse model for human V30M transthyretin. In these studies, Anakinra decreased, among other markers, nerve levels of IL-1b, NF-B and activated-caspase 3, associated with a decrease in TTRnon fibrillar deposition. We compared the efficacy of other compounds under human therapeutical trials for Familial Amyloidotic Polyneuropathy (FAP) in the same animal model, having 5 months of age
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