ArticleNeuroscience letters2021
Vorinostat, a histone deacetylase inhibitor, ameliorates the sociability and cognitive memory in an Ash1L-deletion-induced ASD/ID mouse model.
Article in Neuroscience letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A machine learning-enabled blood transcriptomic signature for digital diagnosis and subtyping of Alzheimer's disease.NPJ digital medicine · 2026Article
- Exploring key genes and pathways associated with sex differences in autism spectrum disorder: integrated bioinformatic analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Review
- Increasing histone acetylation improves sociability and restores learning and memory in KAT6B-haploinsufficient mice.The Journal of clinical investigation · 2024Article
- Review
- The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities.Frontiers in neuroscience · 2023Review
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Authors and funding
4 authors.
Funding
Abstract
Autism spectrum disorder (ASD) and intellectual disability (ID) are neurodevelopmental diseases associated with various gene mutations. Previous genetic and clinical studies reported that ASH1L is a high ASD risk gene identified in human patients. Our recent study used a mouse model to demonstrate that loss of ASH1L in the developing mouse brain was sufficient to cause multiple developmental defects, core autistic-like behaviors, and impaired cognitive memory, suggesting that the disruptive ASH1L mutations are the causative drivers leading the human ASD/ID genesis. Using this Ash1L-deletion-induced ASD/ID mouse model, here we showed that postnatal administration of vorinostat (SAHA), a histone deacetylase inhibitor (HDACi), significantly ameliorated both ASD-like behaviors and ID-like cognitive memory deficit. Thus, our study demonstrates that SAHA is a promising reagent for the pharmacological treatment of core ASD/ID behavioral and memory deficits caused by disruptive ASH1L mutations.
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