Another study showed that blocking the IL-1 receptor (IL-1R) alleviated cognitive deficit, partly reduced fibrillar Aβ formation, significantly attenuated tauopathies, and restored neuronal β-catenin pathway in the 3xTg-AD mouse model of AD (a triple-transgenic model with three mutant human genes: APPswe, PS1M146V, and tauP301L) [76]. This evidence concerns the gene IL1R1 and Alzheimer disease.