An increase in Aβ load accelerates disease progression and drives tau pathology, ultimately leading to neurodegeneration in AD.[1] To determine whether the cognitive function improvements observed with LDIR were associated with the reductions in Aβ load, we performed immunostaining using 6E10 antibodies to visualize Aβ deposits in the subiculum area of 15 months old aged 3xTg‐AD mice after 3.5 months of X‐ray treatment (400 mGy). Here, MAPT is linked to Alzheimer disease.