This is consistent with results showing that specific small-molecule ligands that bind to S2R displace endogenous β-amyloid oligomers from human brain samples from individuals with Alzheimer’s disease, displace β-amyloid oligomer binding to primary cultured neurons, and reverse cognitive deficits in Alzheimer model mice [2,3]. The gene discussed is TMEM97; the disease is early-onset autosomal dominant Alzheimer disease.