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Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia
Graham NS, Sharp DJ.. Journal of neurology, neurosurgery, and psychiatry, 2019-09-21
Topic: Risk, prevention and care in population studies
Traumatic brain injury (TBI) leads to increased rates of dementia, including Alzheimer's disease. The mechanisms by which trauma can trigger neurodegeneration are increasingly understood. For example, diffuse axonal injury is implicated in disrupting microtubule function, providing the potential context for pathologies of tau and amyloid to develop. The neuropathology of post-traumatic dementias is increasingly well characterised, with recent work focusing on chronic traumatic encephalopathy (CTE). However, clinical diagnosis of post-traumatic dementia is problematic. It is often difficult to disentangle the direct effects of TBI from those produced by progressive neurodegeneration or other post-traumatic sequelae such as psychiatric impairment. CTE can only be confidently identified at postmortem and patients are often confused and anxious about the most likely cause of their post-traumatic problems. A new approach to the assessment of the long-term effects of TBI is needed. Accurate methods are available for the investigation of other neurodegenerative conditions. These should be systematically employed in TBI. MRI and positron emission tomography neuroimaging provide biomarkers of neurodegeneration which may be of particular use in the postinjury setting. Brain atrophy is a key measure of disease progression and can be used to accurately quantify neuronal loss. Fluid biomarkers such as neurofilament light can complement neuroimaging, representing sensitive potential methods to track neurodegenerative processes that develop after TBI. These biomarkers could characterise endophenotypes associated with distinct types of post-traumatic neurodegeneration. In addition, they might profitably be used in clinical trials of neuroprotective and disease-modifying treatments, improving trial design by providing precise and sensitive measures of neuronal loss.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Graham, N. S., & Sharp, D. J. (2019). Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia. Journal of neurology, neurosurgery, and psychiatry. https://doi.org/10.1136/jnnp-2017-317557
Vancouver
Graham NS, Sharp DJ. Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia. Journal of neurology, neurosurgery, and psychiatry. 2019. doi:10.1136/jnnp-2017-317557. PMID: 31542723.
BibTeX
@article{graham2019-31542723,
author = {Graham, N. S. and Sharp, D. J.},
title = {{Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia}},
journal = {Journal of neurology, neurosurgery, and psychiatry},
year = {2019},
doi = {10.1136/jnnp-2017-317557},
pmid = {31542723},
url = {https://doi.org/10.1136/jnnp-2017-317557}
}
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Key findings
- These biomarkers could characterise endophenotypes associated with distinct types of post-traumatic neurodegeneration.
Why it matters
This review describes that traumatic brain injury leads to increased rates of dementia, including Alzheimer's disease, and that the mechanisms by which trauma can trigger neurodegeneration are increasingly understood. It notes that clinical diagnosis of post-traumatic dementia is problematic and that a new approach to assessment is needed, with biomarkers such as MRI and positron emission tomography neuroimaging potentially useful.
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Study details
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neurology, neurosurgery, and psychiatry) |
| Journal's citation record | 3 / 4 | Journal of Neurology Neurosurgery & Psychiatry: journal h-index 336 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 341 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 37.9 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 5 / 6 | Cited 20.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 3 / 4 | Cited 155 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author David Sharp: h-index 86 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Imperial College London: institution h-index 1,744 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31542723) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
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Read the original
- DOI: 10.1136/jnnp-2017-317557
- PubMed: 31542723
- Original source →
- Free full text: Journal of Neurology Neurosurgery & Psychiatry →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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