Evidence map›Paper›PMID 21312009›Full record

ReviewCurrent psychiatry reports2011

Power and pitfalls of the genome-wide association study approach to identify genes for Alzheimer's disease.

Richard Sherva, Lindsay A Farrer

Abstract readReview
In one paragraph

Review in Current psychiatry reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Precision pharmacology for Alzheimer's disease.Pharmacological research · 2018
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

2 authors.

Richard ShervaDepartment of Medicine (Biomedical Genetics), Boston University School of Medicine, Boston, MA 02118, USA.
Lindsay A Farrer

Funding

Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
EPIDEMIOLOGY OF DEMENTIA IN THE FRAMINGHAM STUDYR01AG008122 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, SESHADRI, SUDHA · 1989 to 2015
$14.4M
Genetics of Alzheimer's Disease in Israeli ArabsR01AG017173 · NIA · UNIVERSITY OF LOUISVILLE · PI FRIEDLAND, ROBERT PAUL · 2005 to 2009
$5.4M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
Multi-ethnic genome-wide Alzheimer's association studyR01AG025259 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FARRER, LINDSAY A. · 2006 to 2010
$2.6M
GENETICS OF ALZHEIMER'S DISEASE IN ISRAELI ARABSU01AG017173 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI FRIEDLAND, ROBERT PAUL · 2000 to 2004
$1.7M
NIA NIH HHS P30 AG013846NIA NIH HHS R01 AG008122NIA NIH HHS R01 AG017173NIA NIH HHS R01 AG025259NIA NIH HHS R01 AG033193NIA NIH HHS U01 AG017173NIA NIH HHS U01 AG032984
6 · The paper itself

Abstract

Until recently, the search for genes contributing to Alzheimer's disease (AD) had been slow and disappointing, with the notable exception of the APOE ε4 allele, which increases risk and reduces the age at onset of AD in a dose-dependent fashion. Findings from genome-wide association studies (GWAS) made up of fewer than several thousand cases and controls each have not been replicated. Efforts of several consortia--each assembling much larger datasets with sufficient power to detect loci conferring small changes in AD risk--have resulted in robust associations with many novel genes involved in multiple biological pathways. Complex data mining strategies are being used to identify additional members of these pathways and gene-gene interactions contributing to AD risk. Guided by GWAS results, next-generation sequencing and functional studies are under way with the hope of helping us better understand AD pathology and providing new drug targets.

Indexed as

Genetic Predisposition to DiseaseAllelesAlzheimer DiseaseApolipoproteins EGenetic LociGenome-Wide Association StudyHumansPolymorphism, Single NucleotideApolipoproteins E

Identifiers

PMID21312009
PMCPMC3154249

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.