Therefore, the neuronal stress conditions, triggered by the severe pathology in 18-month-old 3×Tg-AD mice, could increase the PDIA3 expression levels as well as the PDIA3-dependent redox-sensor activity on mTORC1, further contributing to its dysregulation, and thus worsening the AD-like neuropathology. Here, PDIA3 is linked to Alzheimer disease.