This drug has revealed selective deleterious roles of TNF-R1 in animal models of Parkinson’s disease [72, 73], Alzheimer’s disease [74], and autoimmune encephalomyelitis [75], Previously, we used XPro1595 and a variety of biochemical approaches to show that soluble TNF/TNF-R1 interactions contributes to cognitive decline, neuronal Ca2+ dysregulation, and altered synaptic plasticity in aged rats [34]. The gene discussed is TNF; the disease is early-onset autosomal dominant Alzheimer disease.