This interaction assessed biophysically, in the postmortem brain from individuals with Alzheimer’s disease, corroborates in vitro and in vivo evidence of displacement of amyloid-β oligomers [64], representing a potential mechanism of action underlying the protection against amyloid-β oligomer-induced synaptic degradation [153,154,155,156,157] observed with S2R modulators [64]. This evidence concerns the gene TMEM97 and early-onset autosomal dominant Alzheimer disease.