Because we did not see a significant neuropathological increase between 6‐ and 12‐month‐old 3xTg‐AD hippocampus, the increase of dysregulated CCC at 12 months could be explained by some of the known “hallmarks of AD,” including age‐associated loss of proteostasis, extended duration of amyloid‐β and tau pathology, and/or widespread pathology as cortical regions show increased neuropathology42 that may affect hippocampal glia–neuron communication. This evidence concerns the gene MAPT and Alzheimer disease.