APP And Neuronal Migration

Main Category: Neurology / Neuroscience
Article Date: 27 Dec 2007 - 0:00 PDT

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Most of the attention directed at â-amyloid precursor protein (APP) has focused on its cleavage and its cleavage products, such as Aâ, one of the hallmarks of Alzheimer's disease.

However, there are clues that full-length APP has important developmental roles. This week, Young-Pearse et al. revisited this issue by knocking down APP using in utero electroporation.

In embryonic day 13 (E13) rat embryos, the authors electroporated APP shRNAs along with a fluorescent reporter and then examined cortical development at E19. The APP shRNA prevented migration of labeled cells from the ventricular zone.

By E30, the labeled cells remained below the cortical plate as a heterotopia. The trapped cells initially expressed neuronal markers, suggesting that the defect was in migration rather than differentiation.

The defect was rescued by full-length APP. In contrast, overexpression of wildtype APP at E13 accelerated migration of labeled cells into the cortical plate.

"Calcium and Vesicle Recruitment at the Calyx of Held"
Tracy L. Young-Pearse, Jilin Bai, Rui Chang, Jessica B. Zheng, Joseph J. LoTurco, and Dennis J. Selkoe
The Journal of Neuroscience, December 26, 2007, 27(52)
Click here to view abstract online

Sara Harris
Society for Neuroscience

Article adapted by Medical News Today from original press release.
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