MAPT and Alzheimer disease: Importantly, the current study demonstrated that these calpeptin‐sensitive cleavages of DLP1 were significantly enhanced by AD‐relevant insults such as treatment with glutamate, soluble Aβ oligomers or okadaic acids, modeling excitotoxicity, Aβ exposure, or tau hyperphosphorylation induction, but not by general insults that disrupt mitochondrial function, which thus demonstrated the involvement of the calpain‐dependent cleavage of DLP1 in AD models.