Overall, the findings presented here provide a strong case against aging-related changes in the total tau levels, somatic tau levels, some phosphorylated forms of tau (i.e., PHF1, AT8, pS422), levels of AIS structural proteins (i.e., AnkG, neurofascin, βIV-spectrin), or AIS morphology within the HP, thus, these factors are unlikely to contribute to the risk of developing AD. This evidence concerns the gene PROS1 and Alzheimer disease.