Amyloid β-protein deposition increases in the brain of MEGF10 Knockout/ AD model mouse

Abstract

Multiple-EGF like domains 10 (MEGF10) is the mammalian homologue of Draper, a phagocytosis receptor of apoptotic cells in Drosophila, and is the type I transmembrane protein that is expressed in the brain. Previously, we clarified that MEGF10 was expressed in neurons and astrocytes, and MEGF10-expressing neurons and astrocytes had the phagocytosis ability of Amyloid β-protein (Aβ) that is thought to be one of the causes of Alzheimer's disease (AD). However, as to whether MEGF10 is involved in Aβ phagocytosis in the brain of AD model mouse was not certain. In this study, we examined this issue using MEGF10 knockout (KO) mouse.

Our results indicated that MEGF10 expression levels in the brain of MEGF10 KO/AD model mice was decreased to less than half compared with that of AD model mice. Furthermore, Aβ deposition and Aβ42 levels were increased in the cortex and hippocampus of MEGF10 KO/ AD model mice.

These results suggested that MEGF10 was contributed to Aβ clearance in the brain of AD model mice.