Of note, a characteristic increase in ERK1/2 activation with an effect size similar to our results has been described for early disease stages of Alzheimer's disease with 25% less ERK1/2 activation in temporal cortex of healthy individuals compared with patients 81, or of ocular ischaemic syndrome where 29% less ERK1 and 21% less ERK2 activation in murine retinae of control mice were found when compared to a mouse model of ocular ischaemic syndrome 82. This evidence concerns the gene MAPK1 and early-onset autosomal dominant Alzheimer disease.