PV interneurons in TgF344-AD rats show early upregulation and increased dendritic complexity 67, and we observe a larger pool of inhibitory neurons recruited by repeated stimulation in ‘AD Impaired’ than in ‘AD Resilient’ rats (Fig. 4C) despite similar total GAD67 NeuN counts (Supplementary Fig. 3B), suggesting hyperexcitable, over-recruited PV cells attempting to compensate for SST loss. The gene discussed is GAD1; the disease is Alzheimer disease.