Answers are grounded in this paper and cite their sources.
Spatial transcriptomics uncover senescence mechanisms in ASD male mouse brains, suggesting new treatments.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder, and maternal immune activation (MIA) is highly implicated in neuropathology and ASD-like phenotypes in offspring. However, the underlying regulatory mechanisms of ASD are multifactorial and remain largely unknown in MIA offspring. Here, we performed spatial transcriptome and single-nucleus RNA sequencing (snRNA-seq) analysis in MIA offspring brain to explore the neurobiological features of ASD. We obtained MIA-induced genes and pathways across multiple key brain regions. We found that senescence-associated APP-CD74 pathway, IGFBP7, and CDKN1A may act as the key pathogenic factors for ASD development. Our further analysis identified broad senescence-associated secretory phenotype (SASP) signature of MIA-induced ASD brain that are regulated in a cell-type specific manner. Moreover, we validated that pharmacological inhibition of IGFBP7 and CDKN1A effectively prevents ASD-like behaviors in MIA offspring. Collectively, our data reveal a senescence-associated regulatory mechanism for ASD, and provide potential intervention strategy for the treatment of ASD.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: