The possible pathological relevance of meprin β for Aβ production was demonstrated in a recent study, which shows that the knock-out of meprin β in a mouse model lacking the APPswe mutations and only harboring the further C-terminal located APP London (APPlon) mutation diminishes Aβ levels and deposition in the mouse brain and rescues cognitive deficits [30]. This evidence concerns the gene MEP1B and Cognitive impairment.