AI Article Synopsis
- - ADNP syndrome is linked to developmental delays, intellectual disabilities, and autism spectrum disorders due to issues with the ADNP transcription factor in mice, particularly the Adnp-haploinsufficient (Adnp-HT) type.
- - Adnp-HT mice exhibit cognitive inflexibility and synaptic plasticity deficits, indicated by hyperactivity of the protein CaMKIIα, affecting their learning and memory capabilities and causing social deficits.
- - In adult Adnp-HT mice, the hippocampus shows elevated levels of phosphorylated CaMKIIα and prolonged long-term potentiation (LTP), which could be countered by inhibiting CaMKIIα, suggesting a link between ADNP deficiency and cognitive issues. *
Article Abstract
ADNP syndrome, involving the ADNP transcription factor of the SWI/SNF chromatin-remodeling complex, is characterized by developmental delay, intellectual disability, and autism spectrum disorders (ASD). Although Adnp-haploinsufficient (Adnp-HT) mice display various phenotypic deficits, whether these mice display abnormal synaptic functions remain poorly understood. Here, we report synaptic plasticity deficits associated with cognitive inflexibility and CaMKIIα hyperactivity in Adnp-HT mice. These mice show impaired and inflexible contextual learning and memory, additional to social deficits, long after the juvenile-stage decrease of ADNP protein levels to ~10% of the newborn level. The adult Adnp-HT hippocampus shows hyperphosphorylated CaMKIIα and its substrates, including SynGAP1, and excessive long-term potentiation that is normalized by CaMKIIα inhibition. Therefore, Adnp haploinsufficiency in mice leads to cognitive inflexibility involving CaMKIIα hyperphosphorylation and excessive LTP in adults long after its marked expressional decrease in juveniles.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10618100 | PMC |
| http://dx.doi.org/10.1038/s41380-023-02129-5 | DOI Listing |
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