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Hippocampal atrophy and apolipoprotein E genotype are independently associated with Alzheimer's disease
Jack CR, Petersen RC, Xu YC, O'Brien PC, Waring SC, Tangalos EG, Smith GE, Ivnik RJ et al.. Annals of neurology, 1998-03-01
Topic: Amyloid, tau and blood-test diagnosis
A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD). One of the strongest imaging associations identified is between AD and hippocampal atrophy. The epsilon4 allele of the apolipoprotein E (ApoE) gene increases the risk of developing AD and lowers the mean age of onset of the disease. The purpose of this study was to assess the association between hippocampal volume and ApoE polymorphisms in elderly control subjects and in patients with probable AD. We performed magnetic resonance imaging-based volume measurements of the hippocampus in 125 cognitively normal elderly controls and 62 patients with probable AD. ApoE genotyping was performed by using standard methods. Hippocampal volumes were significantly smaller in AD cases than in control subjects. Hippocampal volumes did not differ significantly within either clinical group on the basis of ApoE genotype. Both the epsilon4 allele of ApoE and hippocampal atrophy were significantly but independently associated with AD.
Key findings
- A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD).
- Hippocampal volumes were significantly smaller in AD cases than in control subjects.
- Hippocampal volumes did not differ significantly within either clinical group on the basis of ApoE genotype.
- Both the epsilon4 allele of ApoE and hippocampal atrophy were significantly but independently associated with AD.
Study details
- Participants62
- Evidence strengthLow
How this study scored 47/100
Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 27 of the 58 points we could judge it on, which is 47 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Annals of neurology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 1998 — older than 20 years, still counted |
| Sample size | 1 / 4 | 62 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9506546) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 27 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 27 of the 58 points we could judge it on is 47 out of 100. |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Jack, C. R., Petersen, R. C., Xu, Y. C., O'Brien, P. C., Waring, S. C., Tangalos, E. G., et al. (1998). Hippocampal atrophy and apolipoprotein E genotype are independently associated with Alzheimer's disease. Annals of neurology. https://doi.org/10.1002/ana.410430307
Vancouver
Jack CR, Petersen RC, Xu YC, O'Brien PC, Waring SC, Tangalos EG, et al. Hippocampal atrophy and apolipoprotein E genotype are independently associated with Alzheimer's disease. Annals of neurology. 1998. doi:10.1002/ana.410430307. PMID: 9506546.
BibTeX
@article{jack1998-9506546,
author = {Jack, C. R. and Petersen, R. C. and Xu, Y. C. and O'Brien, P. C. and Waring, S. C. and Tangalos, E. G. and Smith, G. E. and Ivnik, R. J. and others},
title = {{Hippocampal atrophy and apolipoprotein E genotype are independently associated with Alzheimer's disease}},
journal = {Annals of neurology},
year = {1998},
doi = {10.1002/ana.410430307},
pmid = {9506546},
url = {https://doi.org/10.1002/ana.410430307}
}
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