Given these prior findings, it is somewhat intriguing in the present study that Igf1r het females, irrespective of AD genotype status, demonstrated higher expression of both iba1 and trem2 levels in cortex, which may indicate altered microglial function, a possibility further supported by the accretion of small plaques when crossed with an amyloidosis model, a finding which is appears to be at odds with a prior report of an attenuation in small plaques in neuronal-specific IGF-1R deletion in APP/PS1 mice. The gene discussed is APP; the disease is Alzheimer disease.