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Amyloid pathology and axonal injury after brain trauma
Scott G, Ramlackhansingh AF, Edison P, Hellyer P, Cole J, Veronese M, Leech R, Greenwood RJ et al.. Neurology, 2016-02-03
Topic: Amyloid, tau and blood-test diagnosis
Objective To image β-amyloid (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer disease (AD). Methods Patients 11 months to 17 years after moderate-severe TBI underwent (11)C-Pittsburgh compound B ((11)C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BPND) images of (11)C-PiB, which index Aβ plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy, was estimated and correlated with (11)C-PiB BPND. Results Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased (11)C-PiB BPND was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy of associated white matter tracts and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum. Conclusions Increased Aβ burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathologic features of dementia, which may relate to axonal damage produced by the injury.
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APA 7th
Scott, G., Ramlackhansingh, A. F., Edison, P., Hellyer, P., Cole, J., Veronese, M., et al. (2016). Amyloid pathology and axonal injury after brain trauma. Neurology. https://doi.org/10.1212/wnl.0000000000002413
Vancouver
Scott G, Ramlackhansingh AF, Edison P, Hellyer P, Cole J, Veronese M, et al. Amyloid pathology and axonal injury after brain trauma. Neurology. 2016. doi:10.1212/wnl.0000000000002413. PMID: 26843562.
BibTeX
@article{scott2016-26843562,
author = {Scott, G. and Ramlackhansingh, A. F. and Edison, P. and Hellyer, P. and Cole, J. and Veronese, M. and Leech, R. and Greenwood, R. J. and others},
title = {{Amyloid pathology and axonal injury after brain trauma}},
journal = {Neurology},
year = {2016},
doi = {10.1212/wnl.0000000000002413},
pmid = {26843562},
url = {https://doi.org/10.1212/wnl.0000000000002413}
}
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Key findings
- Results Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed.
- Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum.
Why it matters
In this small study of 28 participants, long-term survivors of traumatic brain injury showed increased β-amyloid binding in the posterior cingulate cortex and cerebellum compared with controls. The distribution overlapped with but was distinct from Alzheimer disease, so this does not show that traumatic brain injury causes Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 52/100
Published in a leading specialty 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 | 9 / 10 | Tier 2 — leading specialty journal (Neurology) |
| Journal's citation record | 4 / 4 | Neurology: journal h-index 525 (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 | 1 / 5 | 2016 — within 20 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 | 5 / 7 | Cited 149 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.4 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 4 / 6 | Cited 18.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 9 other studies in this library |
| Still being cited | 2 / 4 | Cited 32 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 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26843562) |
| Free to read | 2 / 2 | Free to read |
| Total | 52 / 100 | — |
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