Studies in mice [37–39] have shown that low NPTX2 expression at excitatory synapses of PV interneurons combined with brain amyloidosis is critical for inhibitory circuit dysfunction [12].Thus, a hypothesis emerges whereby a loss of NPTX2-GluA4 synapses in regions affected by amyloidosis may lead to inhibitory circuit dysfunction in AD. The gene discussed is NPTX2; the disease is amyloidosis.