RESUMEN
Neuronal LRRTM3 (leucine-rich repeat transmembrane 3) protein has been reported to promote amyloid-ß protein precursor (AßPP) processing and LRRTM3 is a candidate gene in late-onset Alzheimer's disease. To address the role of LRRTM3 in AßPP processing and amyloid-ß (Aß) production in vivo, we analyzed amyloidogenic processing of AßPP in the brains of LRRTM3-deficient mice and transgenic AßPP/PS1 mice with or without LRRTM3. We did not find differences between the genotypes in the levels of Aß or AßPP C-terminal fragments indicating that LRRTM3 is not an essential regulator of Aß production in adult mice. Moreover, Aß levels in primary cortical neurons were similar between the genotypes, indicating that LRRTM3 is not required for Aß generation in developing mice.
