ReviewMolecular neurodegeneration2025
Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.
Review in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed.
- Traumatic brain injury induces cell-type-specific remodelling of the proteostasis network.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Plasma brain-derived p-Tau217 outperforms other p-Tau species in detecting abnormal brain amyloid in an Asian cohort of older people with cerebrovascular disease burden.The journal of prevention of Alzheimer's disease · 2026Observational
- Bioenergetics of the combat sports brain: Between risk and resilience.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Innovative Biomaterials for Modulating Neuroinflammation and Promoting Repair After Traumatic Brain Injury.Pharmaceutics · 2026Review
- Plasma brain-derived p-tau217 for the identification of amyloid status in a memory clinic cohort.Journal of neurology · 2026Article
- Tau-PET imaging and blood biomarkers reveal early tauopathy in special operations forces exposed to repetitive blast.Brain communications · 2026Article
- Herpes simplex virus infection and Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Mutant Tau (P301L) Enhances Global Protein Translation in Differentiated SH-SY5Y Cells by Upregulating mTOR Signalling.International journal of molecular sciences · 2026Article
- Lithium mitigates hippocampal tau pathology in a rodent model of traumatic brain injury.Acta neuropathologica communications · 2025Article
- Advances in JNK inhibitor development: therapeutic prospects in neurodegenerative diseases and fibrosis.Archives of pharmacal research · 2025Review
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Review
- Traumatic Brain Injury and Dementia: Mechanisms, Risk Stratification, and Clinical Management.Journal of clinical neurology (Seoul, Korea) · 2025Review
- Assessment value of blood pressure variability combined with serum tau protein for the prognosis of patients with traumatic brain injury.Frontiers in neurologyArticle
- Omics-derived biological modules reflect tau positron emission tomography in Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.)Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Tau protein plays a critical role in the physiological functioning of the central nervous system by providing structural integrity to the cytoskeletal architecture of neurons and glia through microtubule assembly and stabilization. Under certain pathological conditions, tau is aberrantly phosphorylated and aggregates into neurotoxic fibrillary tangles. The aggregation and cell-to-cell propagation of pathological tau leads to the progressive deterioration of the nervous system. The clinical entity of traumatic brain injury (TBI) ranges from mild to severe and can promote tau aggregation by inducing cellular mechanisms and signalling pathways that increase tau phosphorylation and aggregation. Chronic traumatic encephalopathy (CTE), which is a consequence of repetitive TBI, is a unique tauopathy characterized by pathological tau aggregates located at the depths of the sulci and surrounding blood vessels. The mechanisms leading to increased tau phosphorylation and aggregation in CTE remain to be fully defined but are likely the result of the primary and secondary injury sequelae associated with TBI. The primary injury includes physical and mechanical damage resulting from the head impact and accompanying forces that cause blood-brain barrier disruption and axonal shearing, which primes the central nervous system to be more vulnerable to the subsequent secondary injury mechanisms. A complex interplay of neuroinflammation, oxidative stress, excitotoxicity, and mitochondrial dysfunction activate kinase and cell death pathways, increasing tau phosphorylation, aggregation and neurodegeneration. In this review, we explore the most recent insights into the mechanisms of tau phosphorylation associated with TBI and propose how multiple cellular pathways converge on tau phosphorylation, which may contribute to CTE progression.
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