Evidence map›Paper›PMID 27433544›Full record

ArticleNeurology. Genetics2016

APOE polymorphisms influence longitudinal lipid trends preceding intracerebral hemorrhage.

Chia-Ling Phuah, Miriam R Raffeld, Alison M Ayres, M Edip Gurol, Anand Viswanathan, Steven M Greenberg, Alessandro Biffi, Jonathan Rosand, Christopher D Anderson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology. Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
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  6. Stroke · 2018
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  8. Pub-Med-dot-com, here we come!Neurology. Genetics · 2016
    Article
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

9 authors at 1 institution in 1 country.

Chia-Ling PhuahDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Miriam R RaffeldDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Alison M AyresDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
M Edip GurolDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Anand ViswanathanDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Steven M GreenbergDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Alessandro BiffiDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Jonathan RosandDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Christopher D AndersonDivision of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Hemorrhagic Stroke Research Group (A.M.A., M.E.G., A.V., S.M.G., J.R., C.D.A.), Division of Behavioral Neurology (A.B.), Division of Psychiatry (A.B.), Department of Psychiatry, Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Broad Institute · US

Funding

The NINDS International Stroke Genetics Consortium StudyU01NS069208 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI KITTNER, STEVEN J · 2010 to 2013
$9.4M
Vascular Dysfunction in Cerebral Amyloid AngiopathyR01AG026484 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2005 to 2019
$7.5M
Gene Discovery for Warfarin-Related Intracerebral HemorrhageR01NS059727 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAND, JONATHAN · 2008 to 2012
$4.2M
Early Detection of Cerebral Amyloid AngiopathyR01NS070834 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2010 to 2014
$2.3M
Harvard Partners Neurology NEXT Clinical Trial SiteU10NS077360 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2011 to 2017
$2.3M
SCORE-IT: The CTA Spot Sign Score in Acute Cerebral HemorrhageR01NS073344 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAND, JONATHAN · 2011 to 2015
$2.2M
Molecular Neuroimaging of Disease Mechanisms in Cerebral Amyloid AngiopathyK23NS083711 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2014 to 2018
$988k
Genetic Analyses of Lipids in Cerebral Hemorrhage and Small Vessel DiseaseK23NS086873 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ANDERSON, CHRISTOPHER DAVID · 2014 to 2018
$951k
Effect of White Matter Disease on Gait and Balance in Cerebral Amyloid AngiopathyK23AG028726 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI VISWANATHAN, ANAND · 2010 to 2014
$823k
NIA NIH HHS K23 AG028726NIA NIH HHS R01 AG026484NINDS NIH HHS K23 NS083711NINDS NIH HHS K23 NS086873NINDS NIH HHS R01 NS059727NINDS NIH HHS R01 NS070834NINDS NIH HHS R01 NS073344NINDS NIH HHS U01 NS069208NINDS NIH HHS U10 NS077360
6 · The paper itself

Abstract

objectiveWe sought to determine whether APOE genotype influences a previously observed decline in serum total cholesterol (TC) and low-density lipoprotein (LDL) levels preceding primary intracerebral hemorrhage (ICH), as a potential demonstration of nonamyloid mechanisms of APOE in ICH risk.

methodsWe performed a single-center retrospective longitudinal analysis using patients with known APOE genotype drawn from an ongoing cohort study of ICH. Serum lipid measurements for TC, triglycerides (TGs), LDL, and high-density lipoprotein (HDL) collected within 2 years before and after index ICH were extracted from electronic medical records. Piecewise linear mixed-effects models were used to compare APOE allele-specific effects on temporal serum lipid trends in ICH. Demographics, medical history, medications, and health maintenance data were included as fixed effects. Inter- and intraindividual variations in lipid levels were modeled as random effects.

resultsA total of 124 ICH cases were analyzed. APOE ε4 carriers had greater rates of decline in serum TC and LDL within 6 months preceding ICH (TC: -7.30 mg/dL/mo, p = 0.0035; LDL: -8.44 mg/dL/mo, p = 0.0001). Conversely, serum TC and LDL levels in APOE ε2 carriers were unchanged within the same time period. APOE genotype had no associations with serum HDL or TG trends.

conclusionsAPOE allele status predicts serum TC and LDL changes preceding acute ICH. Our results have implications for ongoing efforts in dissecting the role of dyslipidemia in cerebrovascular disease risk. APOE genotype-specific influence on lipid trends provides a clue for one mechanism by which APOE may influence risk of ICH. Further characterization of the metabolic roles of APOE is needed to improve the understanding of APOE biology in cerebrovascular disease risk.

Identifiers

PMID27433544
PMCPMC4936477
OpenAlexW2468013017

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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.