Evidence map›Paper›PMID 30798004›Full record

ArticleNeurobiology of disease2019

Assessment of APOE in atypical parkinsonism syndromes.

Marya S Sabir, Cornelis Blauwendraat, Sarah Ahmed, Geidy E Serrano, Thomas G Beach, Matthew Perkins, Ann C Rice, Eliezer Masliah, Christopher M Morris, Lasse Pihlstrom and 11 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Multifaceted roles of APOE in Alzheimer disease.Nature reviews. Neurology · 2024
    Review
  9. Article
  10. Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review.International journal of molecular sciences · 2024
    Review
  11. medRxiv : the preprint server for health sciences · 2023
    Article
  12. Article
  13. Tauopathies: new perspectives and challenges.Molecular neurodegeneration · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Science translational medicine · 2020
    Article
  18. Review
  19. Pathological Influences on Clinical Heterogeneity in Lewy Body Diseases.Movement disorders : official journal of the Movement Disorder Society · 2020
    Review
  20. 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

21 authors at 8 institutions in 3 countries.

Marya S SabirNeurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Cornelis BlauwendraatNeurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Sarah AhmedNeurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Geidy E SerranoCivin Laboratory of Neuropathology, Banner Sun Health Research Institute, Sun City, AZ, USA.
Thomas G BeachCivin Laboratory of Neuropathology, Banner Sun Health Research Institute, Sun City, AZ, USA.
Matthew PerkinsMichigan Brain Bank, University of Michigan Medical School, Ann Arbor, MI, USA.
Ann C RiceVirginia Commonwealth University Brain Bank, Virginia Commonwealth University, Richmond, VA, USA.
Eliezer MasliahLaboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Christopher M MorrisInstitute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.
Lasse PihlstromDepartment of Neurology, Oslo University Hospital, Oslo, Norway.
Alexander PantelyatDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Susan M ResnickLaboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Mark R CooksonLaboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Dena G HernandezLaboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Marilyn AlbertDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Ted M DawsonDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Neuroregeneration and Stem Cell Programs, Institute of Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Liana S RosenthalDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Henry HouldenDepartment of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Olga PletnikovaDepartment of Pathology (Neuropathology), Johns Hopkins University Medical Center, Baltimore, MD, USA.
Juan TroncosoDepartment of Pathology (Neuropathology), Johns Hopkins University Medical Center, Baltimore, MD, USA.
Sonja W ScholzNeurodegenerative Diseases Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: sonja.scholz@nih.gov.
Johns Hopkins University · USNational Institutes of Health · USBanner Sun Health Research Institute · USNewcastle University · GBOslo University Hospital · NOUniversity College London · GBUniversity of Michigan · USVirginia Commonwealth University · US

Funding

Understanding Mechanisms of a-synuclein pathologyP50NS038377 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KO, HANSEOK · 1998 to 2019
$38.8M
'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1985 to 2019
$37.6M
Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI ALEXANDER, GENE E · 2001 to 2020
$32.5M
Early Markers of Alzheimer DiseaseZIAAG000185 · NIA · NATIONAL INSTITUTE ON AGING · PI WALKER, KEENAN · 2009 to 2025
$20.4M
Genetic characterization of atypical parkinsonismZIANS003154 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SCHOLZ, SONJA · 2016 to 2025
$15.4M
Michigan Alzheimer's Disease Core CenterP30AG053760 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIEBERMAN, ANDREW P · 2016 to 2020
$10.1M
Genome wide SNP analysis in Parkinson's diseaseZ01AG000949 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW B · 2006 to 2008
$2.6M
Multi-modal magnetic resonance imaging in progressive supranuclear palsy (PSP)K23AG059891 · NIA · JOHNS HOPKINS UNIVERSITY · PI PANTELYAT, ALEXANDER Y. · 2018 to 2022
$968k
Intramural NIH HHS Z01 AG000949Intramural NIH HHS Z99 NS999999Intramural NIH HHS ZIA NS003154Medical Research Council G0400074Medical Research Council G0502157Medical Research Council G0900652Medical Research Council G1100540NIA NIH HHS K23 AG059891NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG053760NIA NIH HHS P50 AG005146NINDS NIH HHS P50 NS038377
6 · The paper itself

Abstract

Atypical parkinsonism syndromes are a heterogeneous group of neurodegenerative disorders that include corticobasal degeneration (CBD), Lewy body dementia (LBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). The APOE ε4 allele is a well-established risk factor for Alzheimer's disease; however, the role of APOE in atypical parkinsonism syndromes remains controversial. To examine the associations of APOE ε4 and ε2 alleles with risk of developing these syndromes, a total of 991 pathologically-confirmed atypical parkinsonism cases were genotyped using the Illumina NeuroChip array. We also performed genotyping and logistic regression analyses to examine APOE frequency and associated risk in patients with Alzheimer's disease (n = 571) and Parkinson's disease (n = 348). APOE genotypes were compared to those from neurologically healthy controls (n = 591). We demonstrate that APOE ε4 and ε2 carriers have a significantly increased and decreased risk, respectively, of developing Alzheimer's disease (ε4: OR: 4.13, 95% CI: 3.23-5.26, p = 3.67 × 10

Indexed as

AgedAged, 80 and overAllelesAlzheimer DiseaseApolipoproteins EBrainDementiaFemaleGenotypeHumansLewy Body DiseaseMaleMiddle AgedMultiple System AtrophyParkinson DiseaseSupranuclear Palsy, ProgressiveApolipoproteins EAPOEAtypical parkinsonismLewy body dementiaMultiple system atrophyProgressive supranuclear palsy

Identifiers

PMID30798004
PMCPMC6588472
OpenAlexW2917751334

What OpenQuestion holds

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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.