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Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes
Iwata A, Chen XH, McIntosh TK, Browne KD, Smith DH.. Journal of neuropathology and experimental neurology, 2002-12-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Brain trauma has been shown to be a risk factor for developing Alzheimer disease (AD), and AD-like plaques containing amyloid-beta (Abeta) peptides have been found in the brain shortly following trauma. Here, we evaluated the effects of brain trauma on the accumulation of Abeta and expression of amyloid precursor protein (APP) genes (APP695 and APP751/ 770) over 1 yr in a non-transgenic rodent model. Anesthetized male Sprague-Dawley rats were subjected to parasagittal fluid percussion brain injury of moderate severity (2.5-2.9 atm) or sham treatment and their brains were evaluated at 2, 4, 7, 14 days, and 1, 2, 6, 12 months following injury.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Iwata, A., Chen, X. H., McIntosh, T. K., Browne, K. D., & Smith, D. H. (2002). Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes. Journal of neuropathology and experimental neurology. https://doi.org/10.1093/jnen/61.12.1056
Vancouver
Iwata A, Chen XH, McIntosh TK, Browne KD, Smith DH. Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes. Journal of neuropathology and experimental neurology. 2002. doi:10.1093/jnen/61.12.1056. PMID: 12484568.
BibTeX
@article{iwata2002-12484568,
author = {Iwata, A. and Chen, X. H. and McIntosh, T. K. and Browne, K. D. and Smith, D. H.},
title = {{Long-term accumulation of amyloid-beta in axons following brain trauma without persistent upregulation of amyloid precursor protein genes}},
journal = {Journal of neuropathology and experimental neurology},
year = {2002},
doi = {10.1093/jnen/61.12.1056},
pmid = {12484568},
url = {https://doi.org/10.1093/jnen/61.12.1056}
}
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Key findings
- Here, we evaluated the effects of brain trauma on the accumulation of Abeta and expression of amyloid precursor protein (APP) genes (APP695 and APP751/ 770) over 1 yr in a non-transgenic rodent model.
- Anesthetized male Sprague-Dawley rats were subjected to parasagittal fluid percussion brain injury of moderate severity (2.5-2.9 atm) or sham treatment and their brains were evaluated at 2, 4, 7, 14 days, and 1, 2, 6, 12 months following injury.
- Immunohistochemical analysis detected only weak Abeta staining by 2 wk following injury.
- However, by 1 month to 1 yr following injury, strong immunoreactivity for Abeta was found in damaged axons throughout the thalamus and white matter.
Why it matters
In a rat model, brain trauma led to long-term accumulation of amyloid-beta in axons without lasting upregulation of APP genes. This was an animal study, so it does not establish that trauma causes Alzheimer's disease in people or that any intervention prevents it.
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Study details
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2002 — older than 20 years, still counted |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 114 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.4 citations a year over 26 year(s) since 2002 |
| Impact for its field and year | 2 / 6 | Cited 2.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 1 / 4 | Cited 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Douglas H. Smith: h-index 103 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Pennsylvania: institution h-index 1,859 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 12484568) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
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