In this context, the stronger relationship between reactive astrogliosis and tau deposits in the APParc brains, compared to sAD and PSEN1ΔE9 brains [19], could be accounted for by higher exposure to soluble Aβ oligomers—the suggested top culprits of toxicity in AD pathophysiology—and by the fact that Aβ plaque pathology is not a requirement to trigger tau pathology and reactive astrogliosis. This evidence concerns the gene MAPT and Alzheimer disease.