PSEN1 mutations are the most common cause of autosomal dominant Alzheimer’s disease (ADAD). Intriguingly, children carrying a PSEN1-ADAD variant presented high plasma amyloid-β1-42 levels and brain functional hyperconnectivity, indicating a dysregulation at development stages. However, whether there is a neurodevelopmental signature in the adult ADAD brain remains unknown. We aimed to explore neurodevelopment-related genes in the postmortem brain transcriptome of adult PSEN1-ADAD carriers compared to sporadic Alzheimer’s disease (AD). We searched RNA-seq and microarray datasets deposited in GEO for postmortem brain regions vulnerable to AD pathology from PSEN1-ADAD and sporadic early- and late-onset AD (EOAD and LOAD, respectively). We downloaded RNA-seq data from developmental stages in the Brain Span Atlas of the Developing Human Brain. We obtained the differentially expressed genes (DEGs) and DEG-containing gene ontology (GO) terms of biological processes (GOBP) in common between AD subtypes and neurodevelopmental stages. We included 1,998 individuals from 27 datasets. Curiously, all AD subtypes shared DEGs with neurodevelopment, with LOAD brain presenting the highest number mainly in prenatal stages (Figure 1A). We observed neurodevelopment-related GOBP clusters, such as "neurogenesis and gliogenesis" and "embryonic development". The GOBP cluster “neuronal migration” was evidenced only in sporadic EOAD and LOAD. By contrast, PSEN1 carriers presented GOBP terms related to “axon guidance” and “neuronal differentiation” (Figure 1B). Here, we show a neurodevelopmental transcriptomic signature in the autosomal dominant and sporadic adult postmortem AD, regardless of symptom onset or AD genetic inheritance. Our results suggest a neurodevelopment contribution to both sporadic and familial forms of AD.