ReviewMolecular neurobiology2014
Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric comorbidities.
Review in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed.
- Tau Phosphorylation Patterns in the Rat Cerebral Cortex After Traumatic Brain Injury and Sodium Selenate Effects: An Epibios4rx Project 2 Study.Journal of neurotrauma · 2024Article
- Research Progress on the Immune-Inflammatory Mechanisms of Posttraumatic Epilepsy.Cellular and molecular neurobiology · 2023Review
- Volumetric and structural connectivity abnormalities co-localise in TLE.NeuroImage. Clinical · 2022Article
- Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms.Frontiers in aging neuroscience · 2022Review
- Sodium selenate as a therapeutic for tauopathies: A hypothesis paper.Frontiers in aging neuroscience · 2022Article
- The clinical correlation between Alzheimer's disease and epilepsy.Frontiers in neurology · 2022Review
- Article
- Temporal Lobe Epilepsy and Alzheimer's Disease: From Preclinical to Clinical Evidence of a Strong Association.Journal of Alzheimer's disease reports · 2021Review
- An update on the association between traumatic brain injury and Alzheimer's disease: Focus on Tau pathology and synaptic dysfunction.Neuroscience and biobehavioral reviews · 2021Review
- Activation of the Protein Kinase R-Like Endoplasmic Reticulum Kinase (PERK) Pathway of the Unfolded Protein Response after Experimental Traumatic Brain Injury and Treatment with a PERK Inhibitor.Neurotrauma reports · 2021Article
- The Role of Neuroinflammation in Post-traumatic Epilepsy.Frontiers in neurology · 2021Review
- The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments.Current neuropharmacology · 2021Article
- Article
- Prion-Like Propagation Mechanisms in Tauopathies and Traumatic Brain Injury: Challenges and Prospects.Biomolecules · 2020Review
- Catastrophic consequences: can the feline parasite Toxoplasma gondii prompt the purrfect neuroinflammatory storm following traumatic brain injury?Journal of neuroinflammation · 2020Review
- Revisiting the Impact of Neurodegenerative Proteins in Epilepsy: Focus on Alpha-Synuclein, Beta-Amyloid, and Tau.Biology · 2020Review
- Central nervous system lymphatic unit, immunity, and epilepsy: Is there a link?Epilepsia open · 2019Review
- Astrocytic Insulin-Like Growth Factor-1 Protects Neurons Against Excitotoxicity.Frontiers in cellular neuroscience · 2019Article
- Sodium Valproate Ameliorates Neuronal Apoptosis in a Kainic Acid Model of Epilepsy via Enhancing PKC-Dependent GABANeurochemical research · 2018Article
- Tau-Induced Pathology in Epilepsy and Dementia: Notions from Patients and Animal Models.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a common group of neurological diseases. Acquired epilepsy can be caused by brain insults, such as trauma, infection or tumour, and followed by a latent period from several months to years before the emergence of recurrent spontaneous seizures. More than 50% of epilepsy cases will develop chronic neurodegenerative, neurocognitive and neuropsychiatric comorbidities. It is important to understand the mechanisms by which a brain insult results in acquired epilepsy and comorbidities in order to identify targets for novel therapeutic interventions that may mitigate these outcomes. Recent studies have implicated the hyperphosphorylated tubulin-associated protein (tau) in rodent models of epilepsy and Alzheimer's disease, and in experimental and clinical studies of traumatic brain injury. This potentially represents a novel target to mitigate epilepsy and associated neurocognitive and psychiatric disorders post-brain injury. This article reviews the potential role of tau-based mechanisms in the pathophysiology of acquired epilepsy and its neurocognitive and neuropsychiatric comorbidities, and the potential to target these for novel disease-modifying treatments.
Indexed as
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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.