ArticleScientific reports2021
NK1 antagonists attenuate tau phosphorylation after blast and repeated concussive injury.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Pontine pathology mediates common symptoms of blast-induced chronic mild traumatic brain injury.Brain communications · 2026Article
- Neuropeptide and cytokines expression in long COVID-19 related neuropsychological sequelae: insights into NK1R-mediated neuroinflammation andFrontiers in cellular neuroscience · 2026Article
- Domestic violence and chronic traumatic encephalopathy (CTE) - a forensic perspective.Forensic science, medicine, and pathology · 2025Article
- Bidirectional regulation of the brain-gut-microbiota axis following traumatic brain injury.Neural regeneration research · 2025Article
- Brain TRPV1 channel-mediated calcium influx: the immunomodulatory pathway of acupuncture in neuroinflammation.Frontiers in immunology · 2025Review
- The Double-Edged Effects of Substance P in the Pathology of Alzheimer's Disease.Aging and disease · 2024Review
- Experimental laboratory models as tools for understanding modifiable dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Individualized high-resolution analysis to categorize diverse learning and memory deficits in tau rTg4510 mice exposed to low-intensity blast.Frontiers in cellular neuroscience · 2024Article
- Chronic traumatic encephalopathy (CTE)-features and forensic considerations.Forensic science, medicine, and pathology · 2023Article
- Serum tau protein elevation in migraine: a cross-sectional case-control study.The journal of headache and pain · 2023Article
- Blast-Induced Neurotrauma Results in Spatially Distinct Gray Matter Alteration Alongside Hormonal Alteration: A Preliminary Investigation.International journal of molecular sciences · 2023Article
- Effects of a neurokinin-1 receptor antagonist in the acute phase after thoracic spinal cord injury in a rat model.Frontiers in molecular neuroscience · 2023Article
- Neuroprotective Effects of Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells and Monoclonal Antibodies to Neuronal Nitric Oxide Synthase in Brain Pathology Following Alzheimer's Disease Exacerbated by Concussive Head Injury.Advances in neurobiology · 2023Review
- Stem Cell Therapy for Sequestration of Traumatic Brain Injury-Induced Inflammation.International journal of molecular sciences · 2022Review
- Chronic traumatic encephalopathy: genes load the gun and repeated concussion pulls the trigger.Neural regeneration research · 2022Article
- Elevated Substance P Is a Risk Factor for Postoperative Delirium in Patients with Hip Fracture.BioMed research international · 2022Article
- Glial activation and nociceptive neuropeptide elevation associated with the development of chronic post-traumatic headache following repetitive blast exposure.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to repeated concussive traumatic brain injury (TBI) and to blast-induced TBI has been associated with the potential development of the neurodegenerative condition known as chronic traumatic encephalopathy (CTE). CTE is characterized by the accumulation of hyperphosphorylated tau protein, with the resultant tau tangles thought to initiate the cognitive and behavioral manifestations that appear as the condition progresses. However, the mechanisms linking concussive and blast TBI with tau hyperphosphorylation are unknown. Here we show that single moderate TBI, repeated concussive TBI and blast-induced mild TBI all result in hyperphosphorylation of tau via a substance P mediated mechanism. Post-injury administration of a substance P, NK1 receptor antagonist attenuated the injury-induced phosphorylation of tau by modulating the activity of several key kinases including Akt, ERK1/2 and JNK, and was associated with improvement in neurological outcome. We also demonstrate that inhibition of the TRPV1 mechanoreceptor, which is linked to substance P release, attenuated injury-associated tau hyperphosphorylation, but only when it was administered prior to injury. Our results demonstrate that TBI-mediated stimulation of brain mechanoreceptors is associated with substance P release and consequent tau hyperphosphorylation, with administration of an NK1 receptor antagonist attenuating tau phosphorylation and associated neurological deficits. NK1 antagonists may thus represent a pharmacological approach to attenuate the potential development of CTE following concussive and blast TBI.
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