Amyloid beta 1-42 and tau in cerebrospinal fluid after severe traumatic brain injury
Abstract
Objective To determine whether CSF amyloid beta 1-42 (Abeta-42) and tau have predictive value for prognosis after head injury. Methods CSF samples were collected from 29 patients with severe head trauma between 1 and 284 days post-trauma. Abeta-42 and tau levels were measured using sandwich ELISA techniques and compared with CSF levels in patients with cognitive disorders and headache. Results At all time points, concentrations of Abeta-42 were significantly lower in patients with traumatic brain injury (TBI) than in control groups. A significant correlation existed for Abeta-42 levels and outcome of patients. Below a cutoff of 230 pg/mL, the sensitivity of Abeta-42 to discriminate between good outcome (Glasgow Outcome Score 4 and 5) and poor outcome (Glasgow Outcome Score 1 through 3) was 100% at a specificity of 82%. CSF tau levels were significantly higher in patients with TBI than in any control group. In patients with multiple CSF samples collected at various time points between 1 and 32 days after the trauma, tau levels increased early after TBI, peaked in the second week post-trauma, and slowly decreased thereafter. Independent of outcome, all patients had normal tau levels when CSF was collected more than 43 days post-trauma. Conclusions Abeta-42 and tau may play a potential role in the pathophysiology of TBI. Furthermore, the results of this study suggest that Abeta-42 may be a supportive early predictor for recovery after severe head injury.
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Higher cerebral spinal fluid (CSF) levels of Aβ42 predict improved neurological recovery following severe TBI.
“While several clinical studies report that higher cerebral spinal fluid (CSF) levels of Aβ42 predict improved neurological recovery following severe TBI (139, 140)”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [140]
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- Authors
- Franz, G., Beer, R., Kampfl, A., Engelhardt, K., Schmutzhard, E., Ulmer, H., & Deisenhammer, F.
- Affiliations
- Universität Innsbruck (AT)
- Venue
- Neurology
- Published
- 2003-05-13
- Volume
- 60
- Issue
- 9
- Pages
- 1457-1461
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2011984756
- Cited by
- 217
- References
- 32
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 10 · 2023: 5 · 2022: 13 · 2021: 10 · 2020: 13 · 2019: 13 · 2018: 11 · 2017: 21 · 2016: 14 · 2015: 13 · 2014: 12 · 2013: 14 · 2012: 7
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- amyloid-beta 42, tau protein, cerebrospinal fluid biomarkers, severe traumatic brain injury, prognosis, outcome prediction, Glasgow Outcome Scale, early recovery, biomarker kinetics
- MeSH terms
- Adolescent, Adult, Aged, Alzheimer Disease, Brain Damage, Chronic, Brain Injuries, Dementia, Female, Headache, Humans, Male, Peptide Fragments, Retrospective Studies, Risk Factors, Time Factors, Biomarkers, Glasgow Coma Scale, Amyloid beta-Peptides, tau Proteins
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