In fact, in vitro studies showed that attenuation of Alcα function by introducing dominant-negative Alcα or siRNA into cultured cells reduces axonal transport of amyloid precursor protein (APP) to increase cytotoxic Aβ generation9,12, and recent in vivo study showed that Alcα-deficient mice eventually exhibited augmentation of amyloidogenic processing of endogeneous APP sufficient to lead pathologic feature of Alzheimer’s disease such as amyloid plaque formation13. Here, APP is linked to Alzheimer disease.