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A novel, ultrasensitive assay for tau: potential for assessing traumatic brain injury in tissues and biofluids.
Open accessAbstract
Traumatic brain injury (TBI) is a cause of death and disability and can lead to tauopathy-related dementia at an early age. Pathologically, TBI results in axonal injury that is coupled to tau hyperphosphorylation, leading to microtubule instability and tau-mediated neurodegeneration. This suggests that the forms of this protein might serve as neuroinjury-related biomarkers for diagnosis of injury severity and prognosis of the neurological damage prior to clinical expression. We initially determined whether we could detect tau in body fluids using a highly sensitive assay. We used a novel immunoassay, enhanced immunoassay using multi-arrayed fiberoptics (EIMAF) either alone or in combination with rolling circle amplification (a-EIMAF) for the detection of total (T) and phosphorylated (P) tau proteins from brains and biofluids (blood, CSF) of rodents following controlled cortical impact (CCI) and human patients post severe TBI (sTBI). This assay technology for tau is the most sensitive to date with a detection limit of approximately 100 ag/mL for either T-tau and P-tau. In the rodent models, T-tau and P-tau levels in brain and blood increased following CCI during the acute phase and remained high during the chronic phase (30 d). In human CSF samples, T-tau and P-tau increased during the sampling period (5-6 d). T-tau and P-tau in human serum rose during the acute phase and decreased during the chronic stage but was still detectable beyond six months post sTBI. Thus, EIMAF has the potential for assessing both the severity of the proximal injury and the prognosis using easily accessible samples.
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“Tau hyperphosphorylation is also consistently present in the initial and long-term secondary mechanisms initiated by traumatic brain injury (TBI) (Petraglia et al., 2014; Zheng et al., 2014; Rubenstein et al., 2015; Ali et al., 2019; Tan et al., 2020), a leading cause of morbidity and mortality worldwide (Hay et al., 2016).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Rubenstein et al., 2015
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Metadata
- Authors
- Rubenstein, R., Chang, B., Davies, P., Wagner, A. K., Robertson, C. S., & Wang, K. K. W.
- Affiliations
- SUNY Downstate Health Sciences University (US)
- Feinstein Institute for Medical Research (US)
- University of Pittsburgh Medical Center (US)
- Baylor College of Medicine (US)
- University of Florida (US)
- Corresponding author
- Rubenstein, Richard
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2015-03
- Volume
- 32
- Issue
- 5
- Pages
- 342-352
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- PMC
- PMC4348038
- OpenAlex
- W2006643577
- Cited by
- 116
- References
- 90
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 9 · 2023: 14 · 2022: 16 · 2021: 15 · 2020: 11 · 2019: 11 · 2018: 8 · 2017: 12 · 2016: 7 · 2015: 5
- FWCI
- 6.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurotrauma (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- tau protein, tau phosphorylation, traumatic brain injury, biomarkers, rolling circle amplification, cerebrospinal fluid, serum, controlled cortical impact, axonal injury, tauopathy, neurodegeneration, injury severity assessment, prognosis
- MeSH terms
- Animals, Brain Injuries, Humans, Immunoassay, Mice, Inbred C57BL, Sensitivity and Specificity, Immunoblotting, Biomarkers, tau Proteins, Rats, Sprague-Dawley, Mice, Rats
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