Even though this may seem surprising, there is precedent for such an effect: CaMKII also mediates a similar impairment of its own movement that is triggered by amyloid β (Aβ)25,29, one of the major pathological agents in Alzheimer’s disease that also impairs LTP in hippocampal slices30–32. Here, CAMK2G is linked to early-onset autosomal dominant Alzheimer disease.