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 vital developmental roles. that week, Young-Pearse et al. revisited that 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 next

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.

Original post by Mallows