Under excitotoxic age-associated conditions, such as stroke and Alzheimer’s disease, the overactivation of calpains is responsible for TrkB-FL cleavage [73,74], leading to the formation of TrkB-ICD and a transmembrane inactive form of the receptor (TrkB-T’) [74,75]. Here, NTRK2 is linked to early-onset autosomal dominant Alzheimer disease.