ArticleJournal of Alzheimer's disease : JAD2018
Involvement of Activation of Asparaginyl Endopeptidase in Tau Hyperphosphorylation in Repetitive Mild Traumatic Brain Injury.
Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Calpain Inhibitors as Potential Therapeutic Modulators in Neurodegenerative Diseases.Neurochemical research · 2022Pooled it
- 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
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Radiotherapy resistance driven by Asparagine endopeptidase through ATR pathway modulation in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Chronic Neurobehavioral and Neuropathological Consequences of Repeated Blast Exposure in P301S Transgenic Tau Rats.Neurotrauma reports · 2025Article
- Profiling the neuroimmune cascade in 3xTg-AD mice exposed to successive mild traumatic brain injuries.Journal of neuroinflammation · 2024Article
- The Labyrinthine Landscape of APP Processing: State of the Art and Possible Novel Soluble APP-Related Molecular Players in Traumatic Brain Injury and Neurodegeneration.International journal of molecular sciences · 2023Article
- 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
- Hypoxia and the Kynurenine Pathway: Implications and Therapeutic Prospects in Alzheimer's Disease.Oxidative medicine and cellular longevity · 2021Review
- Cornel Iridoid Glycoside Protects Against STAT1-Dependent Synapse and Memory Deficits by IncreasingFrontiers in aging neuroscience · 2021Article
- The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments.Current neuropharmacology · 2021Article
- Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in.Neurobiology of disease · 2020Article
- δ-secretase in neurodegenerative diseases: mechanisms, regulators and therapeutic opportunities.Translational neurodegeneration · 2020Review
- Gene-environment interactions in Alzheimer's disease: A potential path to precision medicine.Pharmacology & therapeutics · 2019Review
- Subacute to chronic Alzheimer-like alterations after controlled cortical impact in human tau transgenic mice.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is an established risk factor for the development of neurodegeneration and dementia late in life. Repetitive mild TBI (r-mTBI) is directly associated with chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disorder characterized by focal perivascular to widespread Alzheimer-type neurofibrillary pathology of hyperphosphorylated tau. Studies in animal models have shown hyperphosphorylation of tau after TBI. However, the molecular mechanisms by which TBI leads to tau pathology are not understood. In this study, we employed western blots and immunohistochemistry to test, in triple-transgenic mouse model of Alzheimer's disease (3xTg-AD), the effect of r-mTBI on tau hyperphosphorylation and activation of asparaginyl endopeptidase (AEP), a cysteine proteinase which is known to be involved in tau hyperphosphorylation. We found that the level of active AEP was increased and correlated with the level of tau hyperphosphorylation following r-mTBI, and that fimbria showed increased immunoreactivity to phospho-tau. In addition, inhibitor 2 of protein phosphatase 2A (I2PP2A) was translocated from neuronal nucleus to the cytoplasm and colocalized with hyperphosphorylated tau. These data suggest the involvement of AEP-I2PP2A-PP2A-ptau pathway in tau pathology in TBI.
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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.