Evidence map›Paper›PMID 20594621›Full record

ReviewNeurobiology of aging2012

The genetic architecture of Alzheimer's disease: beyond APP, PSENs and APOE.

Rita J Guerreiro, Deborah R Gustafson, John Hardy

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 4 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

136 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  16. Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025
    Review
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76 more citing papers are in PubMed but not listed here.

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

3 authors.

Rita J GuerreiroLaboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD, USA. portalegrer@nia.nih.gov
Deborah R Gustafson
John Hardy

Funding

Genetic Analysis Of Alzheimer's DiseaseZ01AG000950 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW · 2002 to 2008
$1.0M
Intramural NIH HHS Z01 AG000950Medical Research Council G0701075Medical Research Council MC_G1000735Medical Research Council MR/K01417X/1NIA NIH HHS Z01 AG000950-06Wellcome Trust 089698
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a complex disorder with a clear genetic component. Three genes have been identified as the cause of early onset familial AD (EOAD). The most common form of the disease, late onset Alzheimer's disease (LOAD), is, however, a sporadic one presenting itself in later stages of life. The genetic component of this late onset form of AD has been the target of a large number of studies, because only one genetic risk factor (APOE4) has been consistently associated with the disease. However, technological advances allow new approaches in the study of complex disorders. In this review, we discuss the new results produced by genome wide association studies, in light of the current knowledge of the complexity of AD genetics.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsApolipoproteins EHumansPresenilin-1Presenilin-2Amyloid beta-Protein PrecursorApolipoproteins EPresenilin-1Presenilin-2PSEN1 protein, humanPSEN2 protein, human

Identifiers

PMID20594621
PMCPMC2980860

What OpenQuestion holds

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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.