Cited by 116Traumatic Brain Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesAlzheimer's disease research and treatments

The DOI matches its Crossref record; 90 of the 90 references it cites were found in a registry or an index.

A novel, ultrasensitive assay for tau: potential for assessing traumatic brain injury in tissues and biofluids.

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Abstract

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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  1. Davies P., 2000, Methods Mol. Med., 32, 361
  2. Hanger D.P., 2007, J. Biochem., 282, 23645
  3. Nowak L.A., 2009, Clin. Neuropathol., 28, 275
  4. Woertgen C., 2002, Acta Neurochir. Suppl, 81, 205

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Items 101–116 of 116

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
Published
2015-03
Volume
32
Issue
5
Pages
342-352
ISSN
  • 0897-7151 (ISSN-L)
  • 1557-9042
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
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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