Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease
Drzezga A, Grimmer T, Henriksen G, Mühlau M, Perneczky R, Miederer I, Praus C, Sorg C et al.. Neurology, 2009-04-01
Topic: Amyloid, tau and blood-test diagnosis
Objective To examine the influence of the APOE genotype on levels of beta-amyloid (Abeta) plaque load and atrophy in patients with Alzheimer disease (AD) in vivo. Methods Thirty-two patients with moderate AD were divided into carriers and noncarriers of the epsilon4 allele. These groups were matched for age, disease duration, education, and cognitive impairment. In all subjects, [11C]PIB-PET was performed for measurement of cerebral Abeta plaque deposition and cranial MRI for the assessment of gray matter volume by voxel-based morphometry (VBM) and for correction of partial volume effects (PVE) in the PET data. Voxel-based comparisons (SPM5) were performed between patient groups and healthy control populations and completed with multiple regression analyses between imaging data and epsilon4 allele frequency. Results Compared to controls, AD-typical patterns of [11C]PIB retention and atrophy were detected in both epsilon4-positive and epsilon4-negative patient groups. In direct comparison, significantly stronger and more extended [11C]PIB uptake was found in epsilon4-positive patients in bilateral temporoparietal and frontal cortex, surviving PVE correction. VBM analysis demonstrated comparable levels of atrophy in both patient groups. Regression analyses revealed a linear association between higher epsilon4 allele frequency and stronger temporoparietal Abeta plaque deposition, independently of other confounds. No major correlation between epsilon4 allele frequency and gray matter decrease was observed. Conclusion These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy. The potential role of Abeta plaque imaging for patient inclusion and follow-up in anti-amyloid therapy trials is strengthened by these findings.
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APA 7th
Drzezga, A., Grimmer, T., Henriksen, G., Mühlau, M., Perneczky, R., Miederer, I., et al. (2009). Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0b013e3181a2e8d0
Vancouver
Drzezga A, Grimmer T, Henriksen G, Mühlau M, Perneczky R, Miederer I, et al. Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease. Neurology. 2009. doi:10.1212/wnl.0b013e3181a2e8d0. PMID: 19339712.
BibTeX
@article{drzezga2009-19339712,
author = {Drzezga, A. and Grimmer, T. and Henriksen, G. and Mühlau, M. and Perneczky, R. and Miederer, I. and Praus, C. and Sorg, C. and others},
title = {{Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease}},
journal = {Neurology},
year = {2009},
doi = {10.1212/wnl.0b013e3181a2e8d0},
pmid = {19339712},
url = {https://doi.org/10.1212/wnl.0b013e3181a2e8d0}
}
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Key findings
- Results Compared to controls, AD-typical patterns of [11C]PIB retention and atrophy were detected in both epsilon4-positive and epsilon4-negative patient groups.
- In direct comparison, significantly stronger and more extended [11C]PIB uptake was found in epsilon4-positive patients in bilateral temporoparietal and frontal cortex, surviving PVE correction.
- VBM analysis demonstrated comparable levels of atrophy in both patient groups.
- Regression analyses revealed a linear association between higher epsilon4 allele frequency and stronger temporoparietal Abeta plaque deposition, independently of other confounds.
- Conclusion These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy.
Why it matters
Among patients with moderate Alzheimer disease, those carrying the APOE epsilon4 allele had stronger and more extended amyloid plaque deposition on PET imaging, while levels of brain atrophy were comparable between carriers and noncarriers. This describes how APOE genotype relates to plaque load in living patients but does not test any therapy.
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Study details
- Evidence strengthLow
How this study scored 46/100
Published in a leading specialty 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 | 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 | 2009 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 248 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.1 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 4 / 6 | Cited 16.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 27 other studies in this library |
| Still being cited | 1 / 4 | Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Alexander Kurz: h-index 38 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Technical University of Munich: institution h-index 1,092 (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 19339712) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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