Evidence map›Paper›PMID 31714636›Full record

SynthesisAnnals of neurology2020

Lipid lowering and Alzheimer disease risk: A mendelian randomization study.

Dylan M Williams, Chris Finan, Amand F Schmidt, Stephen Burgess, Aroon D Hingorani

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Annals of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 4 pooled it
11.9field-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

64 citing papers in PubMed, 4 syntheses or guidelines pooled it, 204 citations in OpenAlex.

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4 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

5 authors at 2 institutions in 3 countries.

Dylan M WilliamsMedical Research Council Unit for Lifelong Health and Ageing at University College London, University College London, London, United Kingdom.ORCID 0000-0002-3825-2487
Chris FinanInstitute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom.
Amand F SchmidtInstitute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom.
Stephen BurgessMedical Research Council Biostatistics Unit, University of Cambridge, Cambridge, United Kingdom.
Aroon D HingoraniInstitute of Cardiovascular Science, Faculty of Population Health, University College London, London, United Kingdom.
University of London · GBUniversity of Cambridge · GB

Funding

British Heart Foundation PG/18/50/33837British Heart Foundation PG/18/5033837British Heart Foundation RG/10/12/28456British Heart Foundation RG/13/13/30194British Heart Foundation RG/18/13/33946Foundation for Geriatric Diseases at Karolinska Institutet 2018-01252Medical Research Council MC_UU_00002/7Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

objectiveTo examine whether genetic variation affecting the expression or function of lipid-lowering drug targets is associated with Alzheimer disease (AD) risk, to evaluate the potential impact of long-term exposure to corresponding therapeutics.

methodsWe conducted Mendelian randomization analyses using variants in genes that encode the protein targets of several approved lipid-lowering drug classes: HMGCR (encoding the target for statins), PCSK9 (encoding the target for PCSK9 inhibitors, eg, evolocumab and alirocumab), NPC1L1 (encoding the target for ezetimibe), and APOB (encoding the target of mipomersen). Variants were weighted by associations with low-density lipoprotein cholesterol (LDL-C) using data from lipid genetics consortia (n up to 295,826). We meta-analyzed Mendelian randomization estimates for regional variants weighted by LDL-C on AD risk from 2 large samples (total n = 24,718 cases, 56,685 controls).

resultsModels for HMGCR, APOB, and NPC1L1 did not suggest that the use of related lipid-lowering drug classes would affect AD risk. In contrast, genetically instrumented exposure to PCSK9 inhibitors was predicted to increase AD risk in both of the AD samples (combined odds ratio per standard deviation lower LDL-C inducible by the drug target = 1.45, 95% confidence interval = 1.23-1.69). This risk increase was opposite to, although more modest than, the degree of protection from coronary artery disease predicted by these same methods for PCSK9 inhibition.

interpretationWe did not identify genetic support for the repurposing of statins, ezetimibe, or mipomersen for AD prevention. Notwithstanding caveats to this genetic evidence, pharmacovigilance for AD risk among users of PCSK9 inhibitors may be warranted. ANN NEUROL 2020;87:30-39.

Indexed as

Mendelian Randomization AnalysisAgedAlzheimer DiseaseApolipoprotein B-100FemaleGenetic Predisposition to DiseaseHumansHydroxymethylglutaryl CoA ReductasesMaleMembrane Transport ProteinsMiddle AgedModels, GeneticPolymorphism, Single NucleotideProprotein Convertase 9APOB protein, humanApolipoprotein B-100HMGCR protein, humanHydroxymethylglutaryl CoA ReductasesMembrane Transport ProteinsNPC1L1 protein, humanPCSK9 protein, humanProprotein Convertase 9

Identifiers

PMID31714636
PMCPMC6944510
OpenAlexW2987364071

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.