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DECOUPLING APP EXPRESSION FROM PLAQUE: EFFECTS OF OVEREXPRESSION OF APPSWIND, PRESENCE OF PLAQUE, AND ROLE OF HERPES VIRUS

      One of the biological roles of amyloid precursor protein (APP), precursor to Abeta plaques, is to attach cargo to motors for axonal transport along microtubules. We identified a 15-aa domain in APP that is sufficient to attach kinesin-1 to fluorescent nano-beads. We also reported that transport is decreased in mice when the APP gene is knocked-out. In old transgenic mice expressing human APPSwInd, linked to Familial Alzheimer’s Disease (FAD), which displays both over-expression of mutated APP and Abeta plaques, axonal transport is altered, as detected by time-lapse manganese-enhanced magnetic resonance imaging (MEMRI) in living mouse brains. Herpes simplex virus (HSV), a predicted risk factor for AD, interacts with the APP-transport system during infectious particle egress, suggesting a possible link between HSV and AD is mediated by dysfunction of the APP transport system.
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