Evidence map›Paper›PMID 17431011›Full record

ArticleAmerican journal of epidemiology2007

Invited commentary: when bad genes look good - APOE*E4, cognitive decline, and diagnostic thresholds.

M Maria Glymour

Abstract readComment
PubMed Publisher
In one paragraph

Article in American journal of epidemiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Alzheimer's disease genetic risk variants beyondAlzheimer's & dementia (Amsterdam, Netherlands) · 2017
    Article
  6. Guidelines for reporting methodological challenges and evaluating potential bias in dementia research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2015
    Review
  7. Article
  8. Selection bias in rheumatic disease research.Nature reviews. Rheumatology · 2014
    Review
  9. Progression of osteoarthritis as a state of inertia.Annals of the rheumatic diseases · 2013
    Article
  10. Review
  11. Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

M Maria GlymourDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA. mg2630@columbia.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Scientific interest frequently focuses on how factors that influence disease onset subsequently affect disease progression. In this commentary, the author discusses four sources of bias that arise in such work. The focus is on Tyas et al.'s analyses (Am J Epidemiol 2007;165:1231-1238) of how the apolipoprotein E *E4 allele, a well-documented risk factor for Alzheimer's disease, influences progression of cognitive impairments from mild or global cognitive impairment to dementia or death. The author addresses four phenomena that can lead to spurious (noncausal) associations between apolipoprotein E *E4 status and rate of progression of cognitive impairments: beginning observations in the middle of a developing pathologic process, survivor bias, uncertainty in the timing of disease diagnosis, and nonlinear disease progression trajectories. Because these sources of bias are potentially relevant in any study of how risk factors for disease onset influence disease progression, the author advocates assessing their likely magnitude in specific contexts when interpreting results.

Indexed as

Research DesignAgedApolipoprotein E4BiasCognition DisordersDementiaDisease ProgressionFemaleHumansNonlinear DynamicsRisk FactorsSurvival AnalysisUncertaintyUnited StatesApolipoprotein E4

Identifiers

PMID17431011

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.