Apparently APP

Apparently APP By Elie Dolgin Axons lose surface APP in the absence of trophic factors. Images Courtesy of A. Nikolaev and M. Tessier-Lavigne Ten years ago, Marc Tessier-Lavigne, a neurobiologist then at the University of California, San Francisco, saw an image he's never forgotten. His postdoc Zhigang He (now at Harvard) showed him a picture of stained mouse embryos indicating that the beta-amyloid precursor protein (APP), a known "bad acto

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By Elie Dolgin

Ten years ago, Marc Tessier-Lavigne, a neurobiologist then at the University of California, San Francisco, saw an image he's never forgotten. His postdoc Zhigang He (now at Harvard) showed him a picture of stained mouse embryos indicating that the beta-amyloid precursor protein (APP), a known "bad actor" in Alzheimer's disease, was highly enriched in neurons and axons during development. Although Tessier-Lavigne never published the finding, the snapshot of the red-tinged embryos "got seared in my brain at the time," he says, telling him that APP might be involved fundamentally in axonal growth or guidance. That memory eventually—and fortuitously—ended up pointing his research towards a potential treatment for the disease.

A couple years back, Tessier-Lavigne and his postdoc Anatoly Nikolaev were studying neuronal expression levels of some 30-odd immunity-related receptors, when they noticed that one—the little-studied "death receptor" DR6—was widely expressed right at the time when neurons are ...

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