Given that GABAB receptors are molecularly and functionally coupled with GIRK channels, mainly the GIRK1 and GIRK2 subunits, in the hippocampus [25,42,51], impairment of presynaptic mechanisms through dysfunction of GABAB-GIRK signalling is likely to greatly influence the activity of neural circuits and can potentially participate in the pathogenesis observed in both P301S and APP/PS1 mouse models of AD. The gene discussed is KCNJ6; the disease is Alzheimer disease.