To counter the influence of TNFR1 signaling, which preferentially responds to soluble, as opposed to transmembrane, TNF, several studies have explored TNFR2 agonism as a therapeutic strategy in animal or in vitro models of Parkinson’s disease [64], neuropathic pain [65], traumatic injury [66], stroke [67] and Alzheimer’s disease [68,69]. This evidence concerns the gene TNFRSF1B and early-onset autosomal dominant Alzheimer disease.