In a recent study, Tracy et al. (55) show that memory loss and LTP impairment in a mouse model of Alzheimer's disease critically depends on reduced synaptic KIBRA levels accompanied by reduced activity-induced postsynaptic actin remodeling and AMPAR insertion, which can be rescued by promoting actin polymerization or by restoring KIBRA expression (55). Here, WWC1 is linked to early-onset autosomal dominant Alzheimer disease.