The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons
Schneider JA, Bienias JL, Wilson RS, Berry-Kravis E, Evans DA, Bennett DA.. Stroke, 2005-03-17
Topic: Brain proteins, microglia and lab models
Background and purpose Studies investigating the relation of the apolipoprotein E (apoE) epsilon4 allele to clinical stroke and to vascular changes on magnetic resonance imaging have been conflicting. Little data are available regarding the relation of apoE epsilon4 to cerebral infarctions documented on postmortem examination. Methods We studied the apoE epsilon4 allele in 214 deceased members of the Religious Orders Study, a longitudinal clinical-pathologic study of aging and Alzheimer disease. The apoE genotype was determined using DNA from lymphocytes. Brains were removed a median of 5 hours (interquartile range, 5.5) after death. At postmortem examination, age, location, and size of macroscopic chronic cerebral infarctions were recorded from 1-cm coronal slabs after paraformaldehyde fixation. We also examined 20-microm paraffin-embedded sections of midfrontal and calcarine cortex for amyloid angiopathy on a scale of 1 to 4. Results Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). Sixty-five subjects (30.4%) had at least 1 apoE epsilon4 allele and 76 (35.5%) exhibited cerebral infarctions. More than 74% of the subjects exhibited amyloid angiopathy with a mean score of 1.4+/-1.2. After controlling for age and sex, apoE epsilon4 increased the odds of cerebral infarction by 2.3-fold (95% CI, 1.2 to 4.2). apoE epsilon4 increased the odds of cortical 3.2-fold (95% CI, 1.3 to 7.7) and subcortical infarctions 2.3-fold (95% CI, 1.2 to 4.5). The effect was unchanged after accounting for amyloid angiopathy. Conclusions apoE epsilon4 increases the odds of chronic cerebral infarction detected at autopsy in older persons.
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APA 7th
Schneider, J. A., Bienias, J. L., Wilson, R. S., Berry-Kravis, E., Evans, D. A., & Bennett, D. A. (2005). The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons. Stroke. https://doi.org/10.1161/01.str.0000160747.27470.2a
Vancouver
Schneider JA, Bienias JL, Wilson RS, Berry-Kravis E, Evans DA, Bennett DA. The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons. Stroke. 2005. doi:10.1161/01.str.0000160747.27470.2a. PMID: 15774818.
BibTeX
@article{schneider2005-15774818,
author = {Schneider, J. A. and Bienias, J. L. and Wilson, R. S. and Berry-Kravis, E. and Evans, D. A. and Bennett, D. A.},
title = {{The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons}},
journal = {Stroke},
year = {2005},
doi = {10.1161/01.str.0000160747.27470.2a},
pmid = {15774818},
url = {https://doi.org/10.1161/01.str.0000160747.27470.2a}
}
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Key findings
- Results Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7).
Why it matters
In 214 deceased participants, carrying the APOE ε4 allele raised the odds of having a cerebral infarction found at autopsy by about 2.3-fold. This links a gene to vascular brain damage but does not test any treatment or prevention.
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Study details
- Study designlongitudinal study
- Participants96
- Effect size30.4%; 35.5%
- Evidence strengthModerate
How this study scored 55/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Stroke) |
| Journal's citation record | 3 / 4 | Stroke: journal h-index 455 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2005 — older than 20 years, still counted |
| Sample size | 1 / 4 | 96 participants |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| 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 | 4 / 7 | Cited 94 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.1 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 2 / 6 | Cited 2.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 2 / 4 | Cited 15 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author David Alan Bennett: h-index 197 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Rush University Medical Center: institution h-index 670 (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 15774818) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 55 / 100 | — |
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