The neuronal transcriptomic profile indicated the significant dysregulation of several key signalling pathways associated with T2D, including phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) signalling (19 DEGs, P = 4.27E−03), cellular senescence (7 DEGs, P = 0.016), cell cycle (9 DEGs, P = 0.024), Alzheimer disease (7 DEGs, P = 0.031), HIF-1 signalling (6 DEGs, P = 0.031), tumour necrosis factor (TNF) signalling (6 DEGs, P = 0.031), oxidative phosphorylation (6 DEGs, P = 0.031), and insulin signalling (8 DEGs, P = 0.039) (Fig. 2). This evidence concerns the gene AKT1 and early-onset autosomal dominant Alzheimer disease.