ArticleNature medicine2014
Alterations in microRNA-124 and AMPA receptors contribute to social behavioral deficits in frontotemporal dementia.
Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 183 citations in OpenAlex.
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- The Ku80-p53-SIRT1 axis in DNA damage response contributes to sporadic and familial ALS and FTD.Nature communications · 2025Article
- Combination of Cas9 and adeno-associated vectors enables efficient in vivo knockdown of precise miRNAs in the rodent and primate brain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- FUS Mislocalization Rewires a Cortical Gene Network to Drive Cognitive and Behavioral Impairment in ALS.medRxiv : the preprint server for health sciences · 2025Article
- A role for astrocytic miR-129-5p in frontotemporal dementia.Translational psychiatry · 2025Article
- Article
- Crucial role of Snf7-3 in synaptic function and cognitive behavior revealed by conventional and conditional knockout mouse models.Neuroscience · 2024Article
- miR-124 coordinates metabolic regulators acting at early stages of human neurogenesis.Communications biology · 2024Article
- DNA Methylation in Autism Spectrum Disorders: Biomarker or Pharmacological Target?Brain sciences · 2024Review
- Exploring the Regulatory Landscape of Dementia: Insights from Non-Coding RNAs.International journal of molecular sciences · 2024Review
- Functional involvement of septal miR-132 in extinction and oxytocin-mediated reversal of social fear.Molecular psychiatry · 2024Article
- Reversible synaptic adaptations in a subpopulation of murine hippocampal neurons following early-life seizures.The Journal of clinical investigation · 2024Article
- Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024Review
- Anti-NMDA and Anti-AMPA Receptor Antibodies in Central Disorders: Preclinical Approaches to Assess Their Pathological Role and Translatability to Clinic.International journal of molecular sciences · 2023Review
- Article
- Preclinical Interventions in Mouse Models of Frontotemporal Dementia Due to Progranulin Mutations.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Astrocyte dysfunction and neuronal network hyperactivity in a CRISPR engineered pluripotent stem cell model of frontotemporal dementia.Brain communications · 2023Article
- Neuronal dysfunction and gene modulation by non-coding RNA in Parkinson's disease and synucleinopathies.Frontiers in cellular neuroscience · 2023Review
- Autophagy and neurodegeneration: Unraveling the role of C9ORF72 in the regulation of autophagy and its relationship to ALS-FTD pathology.Frontiers in cellular neuroscience · 2023Review
49 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
Neurodegenerative diseases, such as frontotemporal dementia (FTD), are often associated with behavioral deficits, but the underlying anatomical and molecular causes remain poorly understood. Here we show that forebrain-specific expression of FTD-associated mutant CHMP2B in mice causes several age-dependent neurodegenerative phenotypes, including social behavioral impairments. The social deficits were accompanied by a change in AMPA receptor (AMPAR) composition, leading to an imbalance between Ca(2+)-permeable and Ca(2+)-impermeable AMPARs. Expression of most AMPAR subunits was regulated by the brain-enriched microRNA miR-124, whose abundance was markedly decreased in the superficial layers of the cerebral cortex of mice expressing the mutant CHMP2B. We found similar changes in miR-124 and AMPAR levels in the frontal cortex and induced pluripotent stem cell-derived neurons from subjects with behavioral variant FTD. Moreover, ectopic miR-124 expression in the medial prefrontal cortex of mutant mice decreased AMPAR levels and partially rescued behavioral deficits. Knockdown of the AMPAR subunit Gria2 also alleviated social impairments. Our results identify a previously undescribed mechanism involving miR-124 and AMPARs in regulating social behavior in FTD and suggest a potential therapeutic avenue.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.