Decreased Sorl1 expression in mice accelerates Aβ production and plaque deposition,17,23 while overexpression of a human SORL1 cDNA significantly reduced the amount of murine Aβ in wild-type mice, and human Aβ in an APP-transgenic mouse model of Alzheimer’s disease.24  Sorl1 haploinsufficiency in mini-pigs induced a cerebrospinal fluid biomarker profile identical to that seen in Alzheimer’s disease.25 The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.