Notably, the T1AM/TAAR1 system has been previously shown to restore LTP in the enthorinal cortex (EC) of mouse models of AD, suggesting that T1AM and TAAR1 are part of an endogenous system that can be modulated to prevent synaptic and behavioral deficits associated with Aβ-related toxicity [41]. Here, TAAR1 is linked to Alzheimer disease.