This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

53/100

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Risk genes beyond APOE

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

In a recent preliminary study it was reported that a severe head injury resulted in the deposition of beta amyloid protein (beta AP) in the cortical ribbon of 30% of patients who survived for less than two weeks. Multiple cortical areas have now been examined from 152 patients (age range 8 weeks-81 years) after a severe head injury with a survival time of between four hours and 2.5 years. This series was compared with a group of 44 neurologically normal controls (age range 51 to 80 years).

What this study adds

Evidence grade: Low

The record lists 152 participants. In this preliminary study, beta amyloid protein deposits were found in one or more cortical areas in 30% of people who died within two and a half years after a severe head injury, and increasing age seemed to increase the extent of these deposits. This suggests that severe head injury can lead to beta amyloid deposition in the brain, but it does not show whether this causes Alzheimer's disease or how to treat, cure, or prevent it.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Roberts, G. W., Gentleman, S. M., Lynch, A., Murray, L., Landon, M., & Graham, D. I. (1994). Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease. Journal of neurology, neurosurgery, and psychiatry. https://doi.org/10.1136/jnnp.57.4.419

Vancouver

Roberts GW, Gentleman SM, Lynch A, Murray L, Landon M, Graham DI. Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease. Journal of neurology, neurosurgery, and psychiatry. 1994. doi:10.1136/jnnp.57.4.419. PMID: 8163989.

BibTeX

@article{roberts1994-8163989,
  author  = {Roberts, G. W. and Gentleman, S. M. and Lynch, A. and Murray, L. and Landon, M. and Graham, D. I.},
  title   = {{Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease}},
  journal = {Journal of neurology, neurosurgery, and psychiatry},
  year    = {1994},
  doi     = {10.1136/jnnp.57.4.419},
  pmid    = {8163989},
  url     = {https://doi.org/10.1136/jnnp.57.4.419}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record lists 152 participants. Ask whether that is enough for the question, and who they were.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Multiple cortical areas have now been examined from 152 patients (age range 8 weeks-81 years) after a severe head injury with a survival time of between four hours and 2.5 years.
This series was compared with a group of 44 neurologically normal controls (age range 51 to 80 years).
Immunostaining with an antibody to beta AP confirmed the original findings that 30% of cases of head injury have beta AP deposits in one or more cortical areas.
Increasing age seemed to accentuate the extent of beta AP deposition and potential correlations with other pathological changes associated with head injury were also investigated.

Why it matters

In this preliminary study, beta amyloid protein deposits were found in one or more cortical areas in 30% of people who died within two and a half years after a severe head injury, and increasing age seemed to increase the extent of these deposits. This suggests that severe head injury can lead to beta amyloid deposition in the brain, but it does not show whether this causes Alzheimer's disease or how to treat, cure, or prevent it.

New to this subject? Start with our plain-English guide: Genetics →

Study details

Participants152
Evidence strengthLow

How this study scored 53/100

Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it. We have no data on institution's track record, so that was left out: it earned 51 of the 97 points we could judge it on, which is 53 out of 100.

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	1 / 5	1994 — older than 20 years, still counted
Sample size	2 / 4	152 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 571 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	16.8 citations a year over 34 year(s) since 1994
Impact for its field and year	4 / 6	Cited 11.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 28 other studies in this library
Still being cited	2 / 4	Cited 23 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author David Ian Graham: h-index 100 (OpenAlex, whole career)
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	0 / 3	OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 8163989)
Free to read	0 / 2	Behind a paywall — scores zero
Points	51 / 97	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 51 of the 97 points we could judge it on is 53 out of 100.
Total	53 / 100	—

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Studies in the library that share something with this one. The line above each title says what.

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

Later studies that cite this one

28 studies in the alzhub library list this one in their references. Showing the 8 highest-scoring.

Related studies in Risk genes beyond APOE from nearby years

Also tagged “precursor”

1,337 studies in the library carry the topic tag “precursor”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 1,337 tagged studies.

Studies sharing this one's topic tags

Similar studies

More on Risk genes beyond APOE

See all studies in Risk genes beyond APOE →