ArticleScience translational medicine2022
TAU ablation in excitatory neurons and postnatal TAU knockdown reduce epilepsy, SUDEP, and autism behaviors in a Dravet syndrome model.
Article in Science translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease.bioRxiv : the preprint server for biology · 2026Article
- Research progress on the relationship between long QT syndrome (LQTS) and epilepsy: A review.Medicine · 2026Review
- SUDEP update 2026: recent advances in experimental and clinical research.Current opinion in neurology · 2026Review
- Beyond microtubule regulation: the multifaceted roles of tau in neuronal function and dysfunction.Translational psychiatry · 2026Review
- Artificial microRNAs targeting tau enable post-symptomatic functional recovery in aged tauopathy mice.Molecular therapy. Nucleic acids · 2026Article
- Pathophysiological Mechanisms Fostering Developmental and Epileptic Encephalopathies (DEE): a Complex Interplay between Genetics, Inflammation and Neurodegeneration.Current neurology and neuroscience reports · 2025Review
- Lacticaseibacillus rhamnosus GR-1 prevents autism-like behaviors by reshaping the maternal and offspring microbiome.NPJ biofilms and microbiomes · 2025Article
- A manifesto for Alzheimer's disease drug discovery in the era of disease-modifying therapies.Molecular neurodegeneration · 2025Review
- Patterns of phosphorylated tau accumulation in a spectrum of acquired and developmental brain lesions associated with refractory epilepsy.Epilepsia · 2025Article
- Exploring biomarkers of neurodegeneration in epilepsy: Critical insights.Epileptic disorders : international epilepsy journal with videotape · 2025Review
- The prevalence of chronic traumatic encephalopathy in a historical epilepsy post-mortem collection.Brain pathology (Zurich, Switzerland) · 2025Article
- CSF Tau Is a Biomarker of Hippocampal Injury in Cryptogenic New-Onset Refractory Status Epilepticus.Annals of clinical and translational neurology · 2025Article
- Spotlight on mechanism of sudden unexpected death in epilepsy in Dravet syndrome.Translational psychiatry · 2025Review
- Astrocytes Lingering at a Crossroads: Neuroprotection and Neurodegeneration in Neurocognitive Dysfunction.International journal of biological sciences · 2025Review
- Activation of the Reelin/GSK-3β/p-Tau Signaling Pathway in the Hippocampus of Patients with Temporal Lobe Epilepsy.Neuropsychiatric disease and treatment · 2025Article
- Dravet syndrome: novel insights intoFrontiers in neuroscience · 2025Review
- Differential effects of tau expression on seizures and epileptogenesis in a mouse model of temporal lobe epilepsy.Frontiers in systems neuroscience · 2025Article
- Evidence that cholinergic mechanisms contribute to hyperexcitability at early stages in Alzheimer's disease.Frontiers in dementia · 2025Review
- Tau reduction with artificial microRNAs modulates neuronal physiology and improves tauopathy phenotypes in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
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14 authors at 2 institutions in 1 country.
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Abstract
Intracellular accumulation of TAU aggregates is a hallmark of several neurodegenerative diseases. However, global genetic reduction of TAU is beneficial also in models of other brain disorders that lack such TAU pathology, suggesting a pathogenic role of nonaggregated TAU. Here, conditional ablation of TAU in excitatory, but not inhibitory, neurons reduced epilepsy, sudden unexpected death in epilepsy, overactivation of the phosphoinositide 3-kinase-AKT-mammalian target of rapamycin pathway, brain overgrowth (megalencephaly), and autism-like behaviors in a mouse model of Dravet syndrome, a severe epileptic encephalopathy of early childhood. Furthermore, treatment with a TAU-lowering antisense oligonucleotide, initiated on postnatal day 10, had similar therapeutic effects in this mouse model. Our findings suggest that excitatory neurons are the critical cell type in which TAU has to be reduced to counteract brain dysfunctions associated with Dravet syndrome and that overall cerebral TAU reduction could have similar benefits, even when initiated postnatally.
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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.