Furthermore, neither full-body nor microglia-selective <i>Gsdmd</i> deletion had an impact on neuronal pathology or the release of pro-inflammatory cytokines.<h4>Conclusion</h4>The absence of key components of the NLRP3 inflammasome pathway did not yield a beneficial effect on tau pathology or neurodegeneration in the preclinical Tau-P301S mouse model of AD. Here, NLRP3 is linked to Alzheimer disease.