It has been shown that Alcα is involved in regulation of amyloidogenic processing of APP: attenuation of Alcα reduces transport of APP to augment cytotoxic Aβ production9,12, and Alcα-deficient mice exhibit enhanced amyloidogenic processing of APP to generate more Aβ sufficient for exacerbating AD related pathogenesis such as amyloid plaque formation13. This evidence concerns the gene APP and Alzheimer disease.