Evidence map›Paper›PMID 23690582›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2013

Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment.

Gwenaëlle Douaud, Helga Refsum, Celeste A de Jager, Robin Jacoby, Thomas E Nichols, Stephen M Smith, A David Smith

Open access · bronzeAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 15 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed, 15 pooled it
42.4field-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

200 citing papers in PubMed, 15 syntheses or guidelines pooled it, 514 citations in OpenAlex.

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  14. Individually modifiable risk factors to ameliorate cognitive aging: a systematic review and meta-analysis.Climacteric : the journal of the International Menopause Society · 2015
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140 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Gwenaëlle DouaudFunctional Magnetic Resonance Imaging of the Brain (FMRIB) Centre, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom. douaud@fmrib.ox.ac.uk
Helga Refsum
Celeste A de Jager
Robin Jacoby
Thomas E Nichols
Stephen M Smith
A David Smith
John Radcliffe Hospital · GBWellcome Centre for Integrative Neuroimaging · GBUniversity of Oxford · GBWarneford Hospital · GB

Funding

Medical Research CouncilWellcome Trust 098369
6 · The paper itself

Abstract

Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented.

Indexed as

Alzheimer DiseaseBayes TheoremEnglandHippocampusHomocysteineHumansImage Processing, Computer-AssistedLinear ModelsLongitudinal StudiesMagnetic Resonance ImagingNerve DegenerationTemporal LobeVitamin B ComplexHomocysteineVitamin B Complexcausal modelingclinical trialdegenerationhippocampusstructural neuroimaging

Identifiers

PMID23690582
PMCPMC3677457
OpenAlexW2113198638

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.