ArticleCell reports2017
ΔFosB Regulates Gene Expression and Cognitive Dysfunction in a Mouse Model of Alzheimer's Disease.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 131 citations in OpenAlex.
- Integrative Transcriptomic and Interactome Analyses Prioritize Candidate Genes for Alzheimer's Disease.Molecular neurobiology · 2026Article
- Voluntary Physical Activity Modulates Brain ΔFOSB and Alters Coactivation Networks in Male and Female Mice.eNeuro · 2026Article
- Reduction of forebrain interneurons alters cellular organization and cortical neurogenesis in a mouse model of X-linked intellectual disability.bioRxiv : the preprint server for biology · 2026Article
- Article
- Repetitive neuronal activation regulates cellular maturation state via nuclear reprogramming.Nature communications · 2026Article
- Sex-dependent interferon signaling contributes to female-biased vulnerability in Alzheimer's disease.Journal of neuroinflammation · 2026Article
- Venezuelan equine encephalitis virus infection causes chronic neurobehavioral outcomes, cellular remodeling, and hippocampal single-cell transcriptomic changes.PLoS pathogens · 2026Article
- Efficient In Vivo Pharmacological Inhibition of ΔFOSB, an AP-1 Transcription Factor, in the Brain.ACS chemical neuroscience · 2026Article
- Multiparity exacerbates Aβ accumulation and promotes cellular senescence in a mouse model of amyloidosis.Immunity & ageing : I & A · 2026Article
- Brain-wide induction of ΔFOSB and altered co-activation networks in a rat model for exercise training.Translational psychiatry · 2026Article
- Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology.Molecular neurodegeneration · 2026Article
- Kv4.2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- A single glucocorticoid response element regulates sociability in a sex-specific manner.Molecular psychiatry · 2026Article
- Chemogenetic activation of hippocampal area CA2 promotes acute and chronic seizures in a mouse model of epilepsy.Neurobiology of disease · 2026Article
- Stereotyped behaviors: behavioral markers of brain dysfunction and welfare impairment in animals.Frontiers in veterinary science · 2026Article
- Article
- Multiomic Analyses Reveal Brainstem Metabolic Changes in a Mouse Model of Dravet Syndrome.Cells · 2025Article
- Chemogenetic activation of hippocampal area CA2 promotes acute and chronic seizures in a mouse model of epilepsy.bioRxiv : the preprint server for biology · 2025Article
- Restoration of sFRP3 Preserves the Neural Stem Cell Pool and Spatial Discrimination Ability in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Immediate-early genes Arc and c-Fos show divergent brain-wide expression following contextual fear conditioning.Communications biology · 2025Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized by cognitive decline and 5- to 10-fold increased seizure incidence. How seizures contribute to cognitive decline in AD or other disorders is unclear. We show that spontaneous seizures increase expression of ΔFosB, a highly stable Fos-family transcription factor, in the hippocampus of an AD mouse model. ΔFosB suppressed expression of the immediate early gene c-Fos, which is critical for plasticity and cognition, by binding its promoter and triggering histone deacetylation. Acute histone deacetylase (HDAC) inhibition or inhibition of ΔFosB activity restored c-Fos induction and improved cognition in AD mice. Administration of seizure-inducing agents to nontransgenic mice also resulted in ΔFosB-mediated suppression of c-Fos, suggesting that this mechanism is not confined to AD mice. These results explain observations that c-Fos expression increases after acute neuronal activity but decreases with chronic activity. Moreover, these results indicate a general mechanism by which seizures contribute to persistent cognitive deficits, even during seizure-free periods.
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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.