ArticleEMBO molecular medicine2022
Acetate supplementation restores cognitive deficits caused by ARID1A haploinsufficiency in excitatory neurons.
Article in EMBO molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Circulating short chain fatty acids in Alzheimer's disease: A cross-sectional observational study.Journal of Alzheimer's disease : JAD · 2025Observational
- Examining structure-activity relationships of ManNAc analogs used in the metabolic glycoengineering of human neural stem cells.Biomaterials advances · 2025Article
- Serum homocysteine showed potential association with cognition and abnormal gut microbiome in major depressive disorder.World journal of psychiatry · 2025Article
- Ageing-associated gut dysbiosis deteriorates mouse cognition.Acta biochimica et biophysica Sinica · 2025Article
- Gut microbiota-derived short chain fatty acids act as mediators of the gut-liver-brain axis.Metabolic brain disease · 2025Review
- SWI/SNF Complex Connects Signaling and Epigenetic State in Cells of Nervous System.Molecular neurobiology · 2025Review
- Loss of microglial Arid1a exacerbates microglial scar formation via elevated CCL5 after traumatic brain injury.Cell communication and signaling : CCS · 2024Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Review
- Clinical outcome and molecular landscape of patients with ARID1A-loss gastric cancer.Cancer science · 2024Article
- Abnormal chromatin remodeling caused by ARID1A deletion leads to malformation of the dentate gyrus.Cell death and differentiation · 2023Article
- Acetate supplementation restores cognitive deficits caused by ARID1A haploinsufficiency in excitatory neurons.EMBO molecular medicine · 2022Article
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Authors and funding
10 authors.
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Abstract
Mutations in AT-rich interactive domain-containing protein 1A (ARID1A) cause Coffin-Siris syndrome (CSS), a rare genetic disorder that results in mild to severe intellectual disabilities. However, the biological role of ARID1A in the brain remains unclear. In this study, we report that the haploinsufficiency of ARID1A in excitatory neurons causes cognitive impairment and defects in hippocampal synaptic transmission and dendritic morphology in mice. Similarly, human embryonic stem cell-derived excitatory neurons with deleted ARID1A exhibit fewer dendritic branches and spines, and abnormal electrophysiological activity. Importantly, supplementation of acetate, an epigenetic metabolite, can ameliorate the morphological and electrophysiological deficits observed in mice with Arid1a haploinsufficiency, as well as in ARID1A-null human excitatory neurons. Mechanistically, transcriptomic and ChIP-seq analyses demonstrate that acetate supplementation can increase the levels of H3K27 acetylation at the promoters of key regulatory genes associated with neural development and synaptic transmission. Collectively, these findings support the essential roles of ARID1A in the excitatory neurons and cognition and suggest that acetate supplementation could be a potential therapeutic intervention for CSS.
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