ArticleFrontiers in neurology2023
Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer's disease, and epilepsy.
Article in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- The Role of Photobiomodulation to Modulate Ion Channels in the Nervous System: A Systematic Review.Cellular and molecular neurobiology · 2024Pooled it
- Post-traumatic stress disorder: pathogenesis, epidemiological characteristics, animal models, and potential therapeutic strategies.Military Medical Research · 2026Review
- Tau protein as a regulator of mitochondrial function and dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting mtDNA to Modulate Mitochondrial Dysfunction in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Neurodegeneration Biomarkers in Epilepsy: A Critical Review of Current Findings.Life (Basel, Switzerland) · 2026Review
- Bioenergetic failure and oxidative stress: mitochondrial contributions to Alzheimer's disease.Inflammopharmacology · 2025Review
- Patterns of phosphorylated tau accumulation in a spectrum of acquired and developmental brain lesions associated with refractory epilepsy.Epilepsia · 2025Article
- CSF Tau Is a Biomarker of Hippocampal Injury in Cryptogenic New-Onset Refractory Status Epilepticus.Annals of clinical and translational neurology · 2025Article
- Breaking the Barrier: The Role of Proinflammatory Cytokines in BBB Dysfunction.International journal of molecular sciences · 2025Review
- Alzheimer's Disease and Epilepsy: Exploring Shared Pathways and Promising Biomarkers for Future Treatments.Journal of clinical medicine · 2024Review
- Understanding epileptogenesis from molecules to network alteration.Encephalitis (Seoul, Korea) · 2024Article
- Peripheral oxidative stress related biomarkers in Alzheimer's disease: A systematic review of their implications for diagnosis and disease monitoring.Alzheimer's & dementia (Amsterdam, Netherlands)Review
- Pharmacological Intervention of Post-traumatic Seizure: Advanced Research Progress.Dose-response : a publication of International Hormesis SocietyReview
- Assessment value of blood pressure variability combined with serum tau protein for the prognosis of patients with traumatic brain injury.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI), Alzheimer's disease (AD), and epilepsy share proposed mechanisms of injury, including neuronal excitotoxicity, cascade signaling, and activation of protein biomarkers such as tau. Although tau is typically present intracellularly, in tauopathies, phosphorylated (p-) and hyper-phosphorylated (hp-) tau are released extracellularly, the latter leading to decreased neuronal stability and neurofibrillary tangles (NFTs). Tau cleavage at particular sites increases susceptibility to hyper-phosphorylation, NFT formation, and eventual cell death. The relationship between tau and inflammation, however, is unknown. In this review, we present evidence for an imbalanced endoplasmic reticulum (ER) stress response and inflammatory signaling pathways resulting in atypical p-tau, hp-tau and NFT formation. Further, we propose tau as a biomarker for neuronal injury severity in TBI, AD, and epilepsy. We present a hypothesis of tau phosphorylation as an initial acute neuroprotective response to seizures/TBI. However, if the underlying seizure pathology or TBI recurrence is not effectively treated, and the pathway becomes chronically activated, we propose a "tipping point" hypothesis that identifies a transition of tau phosphorylation from neuroprotective to injurious. We outline the role of amyloid beta (Aβ) as a "last ditch effort" to revert the cell to programmed death signaling, that, when fails, transitions the mechanism from injurious to neurodegenerative. Lastly, we discuss targets along these pathways for therapeutic intervention in AD, TBI, and epilepsy.
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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.