In the mouse model of Alzheimer’s disease, the deletion of trpc1 gene was found to aggravate amyloid-β (Aβ)-induced learning and memory deficits and TRPC1 was shown to interact with Aβ precursor protein (APP) at the transmembrane region, resulting in reduced Aβ levels in hippocampal neurons and attenuation of apoptosis (Li et al., 2018). Here, APP is linked to early-onset autosomal dominant Alzheimer disease.