Although AD mice exhibited the expected hyperlocomotive phenotype during OF testing, spatial memory performance was not significantly different between WT and AD p38+/+ groups at the age tested, indicating (a) that we are modeling a pre-clinical phase of the disease wherein overall cognitive function is unimpaired despite the presence of amyloid pathology [43], and (b) substantial loss of microglial p38α signaling is not detrimental to at least this type of spatial memory. The gene discussed is MAPK14; the disease is amyloidosis.