Evidence map›Paper›PMID 31272697›Full record

ArticleNeurobiology of aging2019

Genetic risk for coronary heart disease alters the influence of Alzheimer's genetic risk on mild cognitive impairment.

Jeremy A Elman, Matthew S Panizzon, Mark W Logue, Nathan A Gillespie, Michael C Neale, Chandra A Reynolds, Daniel E Gustavson, Brinda K Rana, Ole A Andreassen, Anders M Dale and 3 more

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

Article in Neurobiology of aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

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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

13 authors at 6 institutions in 2 countries.

Jeremy A ElmanDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA. Electronic address: jaelman@ucsd.edu.
Matthew S PanizzonDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA.
Mark W LogueNational Center for PTSD: Behavioral Science Division, VA Boston Healthcare System, Boston, MA, USA; Department of Psychiatry and the Biomedical Genetics Section, Boston University School of Medicine, Boston, MA, USA; Department of Biostatistics, Boston University School of Public Health, Boston MA, USA.
Nathan A GillespieVirginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University, Richmond, VA, USA.
Michael C NealeVirginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University, Richmond, VA, USA.
Chandra A ReynoldsDepartment of Psychology, University of California, Riverside, CA, USA.
Daniel E GustavsonDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA.
Brinda K RanaDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA.
Ole A AndreassenNORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo and Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway.
Anders M DaleCenter for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA; Department of Radiology, University of California, San Diego, La Jolla, CA, USA; Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA.
Carol E FranzDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA.
Michael J LyonsDepartment of Psychological and Brain Sciences, Boston University, Boston, MA, USA.
William S KremenDepartment of Psychiatry University of California, San Diego, La Jolla, CA, USA; Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA; Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System, La Jolla, CA, USA.
University of California, San Diego · USBoston University · USVirginia Commonwealth University · USOslo University Hospital · NOUniversity of California, Riverside · USVA San Diego Healthcare System · US

Funding

The VETSA Longitudinal Twin Study of Cognition and Aging (VETSA 4)R01AG050595 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ELMAN, JEREMY A, FRANZ, CAROL ELAINE · 2015 to 2024
$28.0M
The VETSA Longitudinal MRI Twin Study of AgingR01AG022381 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KREMEN, WILLIAM S. · 2003 to 2019
$22.3M
Effects of Androgen Deprivation Therapy on Preclinical Symptoms of Alzheimer's DiseaseR01AG056410 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PANIZZON, MATTHEW S · 2017 to 2021
$3.3M
Testosterone-Androgen Receptor Genetics: Role in Cognitive and Biological AgingK08AG047903 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PANIZZON, MATTHEW S · 2014 to 2017
$452k
Archiving the Vietnam Era Twin Studies of Aging (VETSA): New Uses for Old DataR03AG046413 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FRANZ, CAROL ELAINE · 2013 to 2014
$247k
NIA NIH HHS K08 AG047903NIA NIH HHS R01 AG022381NIA NIH HHS R01 AG050595NIA NIH HHS R01 AG056410NIA NIH HHS R03 AG046413
6 · The paper itself

Abstract

Understanding genetic influences on Alzheimer's disease (AD) may improve early identification. AD polygenic risk scores (AD-PRSs) are associated with increased odds of AD and mild cognitive impairment (MCI). Additional sources of genetic risk may also contribute to disease outcomes. Coronary artery disease (CAD) is a risk factor for AD, interacts with AD pathology, and is also heritable. We showed that incidence-based and prevalence-based CAD-PRSs moderate the association between the AD-PRS and MCI, but in opposing directions. Higher incidence-based CAD-PRSs interacted with the AD-PRS to further increase MCI risk. Conversely, the AD-PRS was predictive of MCI when prevalence-based CAD-PRSs were low. The latter finding is likely due to prevalent CAD cases being biased toward longer postevent survival times, perhaps selecting for protective loci that offset AD risk. These results demonstrate (1) the importance of examining multiple PRSs and their interactions; (2) how genetic risk for one disease can modify the impact of genetic risk for another; and (3) the importance of considering ascertainment procedures of GWAS used for genetic risk prediction.

Indexed as

Alzheimer DiseaseCognitive DysfunctionCoronary DiseaseRiskAlzheimer's diseaseCognitive impairmentCoronary artery diseaseIncidence-prevalence biasNeyman biasPolygenic risk scores

Identifiers

PMID31272697
PMCPMC6899214
OpenAlexW2951468689

What OpenQuestion holds

Textmetadata
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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.