Notably, it has been shown previously that producing Aβ42 and BRICHOS at equimolar amounts from a common precursor in transgenic mice results in unaltered plaque load but markedly reduced oligomer formation and no cognitive decline compared to when Aβ42 is produced form APP without any BRICHOS overexpression.60 Also, transgenic overexpression of BRICHOS in APP/presenilin 1 mutant mice results in modest reduction in plaque load but marked reduction in GFAP levels and improved cognition.61 This evidence concerns the gene APP and Mental deterioration.