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 early-onset autosomal dominant Alzheimer disease.