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Role of genes and environments for explaining Alzheimer disease
Gatz M, Reynolds CA, Fratiglioni L, Johansson B, Mortimer JA, Berg S, Fiske A, Pedersen NL.. Archives of general psychiatry, 2006-02-01
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Context Twin studies using selected samples have shown high heritability for Alzheimer disease (AD). Objective To evaluate genetic and environmental influences on AD in a fully ascertained population of older twins, including like- and unlike-sex pairs. Design Five-group quantitative genetic model: male monozygotic twins, female monozygotic twins, male dizygotic twins, female dizygotic twins, and unlike-sex twins. Setting and participants All twins in the Swedish Twin Registry aged 65 years and older. The study included 11,884 twin pairs, among whom were 392 pairs in which 1 or both members had AD. Main outcome measures All individuals were screened for cognitive dysfunction. Suspected cases of dementia and their co-twins received complete clinical diagnostic evaluations for AD. Estimates of heritability, shared environmental influences, and nonshared environmental influences, adjusting for age, were derived from the twin data. Results Heritability for AD was estimated to be 58% in the full model and 79% in the best-fitting model, with the balance of variation explained by nonshared environmental influences. There were no significant differences between men and women in prevalence or heritability after controlling for age. Within pairs concordant for AD, intrapair difference in age at onset was significantly greater in dizygotic than in monozygotic pairs, suggesting genetic influences on timing of the disease. Conclusions In the largest twin study to date, we confirmed that heritability for AD is high and that the same genetic factors are influential for both men and women. However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset.
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APA 7th
Gatz, M., Reynolds, C. A., Fratiglioni, L., Johansson, B., Mortimer, J. A., Berg, S., et al. (2006). Role of genes and environments for explaining Alzheimer disease. Archives of general psychiatry. https://doi.org/10.1001/archpsyc.63.2.168
Vancouver
Gatz M, Reynolds CA, Fratiglioni L, Johansson B, Mortimer JA, Berg S, et al. Role of genes and environments for explaining Alzheimer disease. Archives of general psychiatry. 2006. doi:10.1001/archpsyc.63.2.168. PMID: 16461860.
BibTeX
@article{gatz2006-16461860,
author = {Gatz, M. and Reynolds, C. A. and Fratiglioni, L. and Johansson, B. and Mortimer, J. A. and Berg, S. and Fiske, A. and Pedersen, N. L.},
title = {{Role of genes and environments for explaining Alzheimer disease}},
journal = {Archives of general psychiatry},
year = {2006},
doi = {10.1001/archpsyc.63.2.168},
pmid = {16461860},
url = {https://doi.org/10.1001/archpsyc.63.2.168}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Results Heritability for AD was estimated to be 58% in the full model and 79% in the best-fitting model, with the balance of variation explained by nonshared environmental influences.
- There were no significant differences between men and women in prevalence or heritability after controlling for age.
- Within pairs concordant for AD, intrapair difference in age at onset was significantly greater in dizygotic than in monozygotic pairs, suggesting genetic influences on timing of the disease.
Why it matters
In all twins aged 65 and over in the Swedish Twin Registry (11,884 pairs, 392 with Alzheimer's in one or both twins), genetic differences accounted for an estimated 58% to 79% of the variation in who developed Alzheimer's, depending on the model. The rest was attributed to environmental factors not shared by twins. Heritability did not differ significantly between men and women, and the timing of onset also appeared to be partly genetic. These are population-level estimates from one country, not a measure of any individual's risk, and the study does not identify genes or test any treatment.
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Study details
- Participants11,884
- Evidence strengthLow
How this study scored 64/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Archives of general psychiatry) |
| Journal's citation record | 4 / 4 | Archives of General Psychiatry: journal h-index 543 (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 | 2006 — older than 20 years, still counted |
| Sample size | 4 / 4 | 11,884 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 | 7 / 7 | Cited 1,804 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 82.0 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 5 / 6 | Cited 28.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 5 / 6 | Cited by 102 other studies in this library |
| Still being cited | 4 / 4 | Cited 325 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Nancy L. Pedersen: h-index 167 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Southern California: institution h-index 1,521 (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 16461860) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 64 / 100 | — |
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