Evidence map›Paper›PMID 27856775›Full record

ArticleNeurology2016

Genetically decreased vitamin D and risk of Alzheimer disease.

Lauren E Mokry, Stephanie Ross, John A Morris, Despoina Manousaki, Vincenzo Forgetta, J Brent Richards

Open access · bronzeAbstract read
In one paragraph

Article in Neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 7 pooled it
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 7 syntheses or guidelines pooled it, 116 citations in OpenAlex.

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  9. Genetics and environmental determinants of Alzheimer's disease and related dementias in older Africans: a narrative review.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 2 countries.

Lauren E MokryFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
Stephanie RossFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
John A MorrisFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
Despoina ManousakiFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
Vincenzo ForgettaFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK.
J Brent RichardsFrom the Department of Epidemiology, Biostatistics and Occupational Health (L.E.M., J.B.R.), Centre for Clinical Epidemiology (L.E.M., S.R., J.A.M., D.M., V.F., J.B.R.), Department of Epidemiology, Lady Davis Institute for Medical Research, Jewish General Hospital, Department of Human Genetics (J.A.M., J.B.R.), and Department of Medicine (D.M., J.B.R.), McGill University, Montreal, Quebec, Canada; and Department of Twin Research and Genetic Epidemiology (J.B.R.), King's College London, UK. brent.richards@mcgill.ca.
King's College London · GB

Funding

National Centralized Repository for Alzheimer's Disease and Related Dementias (NCRAD)U24AG021886 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI TATIANA M. FOROUD · 2002 to 2026
$119.8M
NATIONAL ALZHEIMERS COORDINATING CENTER (NACC)U01AG016976 · NIA · UNIVERSITY OF WASHINGTON · PI KUKULL, WALTER ANTHONY · 1999 to 2020
$72.8M
Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
NIA NIH HHS R01 AG033193NIA NIH HHS U01 AG016976NIA NIH HHS U01 AG032984NIA NIH HHS U24 AG021886Wellcome Trust
6 · The paper itself

Abstract

objectiveTo test whether genetically decreased vitamin D levels are associated with Alzheimer disease (AD) using mendelian randomization (MR), a method that minimizes bias due to confounding or reverse causation.

methodsWe selected single nucleotide polymorphisms (SNPs) that are strongly associated with 25-hydroxyvitamin D (25OHD) levels (p < 5 × 10

resultsThe SUNLIGHT Consortium identified 4 SNPs to be genome-wide significant for 25OHD, which described 2.44% of the variance in 25OHD in CaMos. All 4 SNPs map to genes within the vitamin D metabolic pathway. MR analyses demonstrated that a 1-SD decrease in natural log-transformed 25OHD increased AD risk by 25% (odds ratio 1.25, 95% confidence interval 1.03-1.51, p = 0.021). After sensitivity analysis in which we removed SNPs possibly influenced by pleiotropy and population stratification, the results were largely unchanged.

conclusionsOur results provide evidence supporting 25OHD as a causal risk factor for AD. These findings provide further rationale to understand the effect of vitamin D supplementation on cognition and AD risk in randomized controlled trials.

Indexed as

Alzheimer DiseaseCanadaDietary SupplementsHumansMendelian Randomization AnalysisOsteoporosisPhenotypePolymorphism, Single NucleotideRisk FactorsVitamin DVitamin D

Identifiers

PMID27856775
PMCPMC5207000
OpenAlexW2553553016

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.