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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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