Additionally, a septal nuclei neuron subtype IMN 2-9 (marked by Prdm16 and Ano2) that significantly overexpress in both AD model GMs related to axonogenesis (for example, Nrp1 and Slit2) and synaptogenesis (for example, Ptprd and Nrxn1) (ref. 56) was also significantly expanded in both AD models (Fig. 4f–h), aligning with the observed enlargement of the septal nuclei region several years before the onset of memory decline57. The gene discussed is ANO2; the disease is Alzheimer disease.