Evidence map›Paper›PMID 19906263›Full record

ReviewAnnals of the New York Academy of Sciences2009

Use of genetic variation as biomarkers for Alzheimer's disease.

Christiane Reitz, Richard Mayeux

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06275243 (Alzheimer's Disease as a Sociosanitary Priority), which is not on this map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 16% 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.

NCT06275243 nacompletednot on this mapstarted 2022, after this paper: background citation

Alzheimer's Disease as a Sociosanitary Priority: ApoE Gene Polymorphism

TypeinterventionalSponsorUniversidad de LeónRan2022 to 2024Enrolled511ConditionsAlzheimer DiseaseArmsKit Buccal swab collection & stabilization de Canvax®, Cholesterol levels according to ApoE Genotype, Assessing cardiovascular risk factors in all participants
3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The genetics of Alzheimer's disease.Clinical interventions in aging · 2014
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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 at 1 institution in 1 country.

Christiane ReitzTaub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
Richard Mayeux
Columbia University · US

Funding

Satellite Diagnostic and Treatment Clinic CoreP50AG008702 · NIA · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI DE JAGER, PHILIP L · 1989 to 2019
$46.3M
VASCULAR FACTORS AND MILD COGNITIVE IMPAIRMENT AND ALZHEIMER'S DISEASEP01AG007232 · NIA · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI MANLY, JENNIFER JAIE · 1989 to 2008
$21.7M
Genetic Epidemiology of Alzheimer's Disease in HispanicsR37AG015473 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MAYEUX, RICHARD P · 2004 to 2013
$10.8M
GENETIC EPIDEMIOLOGY OF ALZHEIMERS DISEASE IN HISPANICSR01AG015473 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MAYEUX, RICHARD · 1999 to 2003
$4.6M
Mapping Causative factors in the sortilin-related pathway in Alzheimer's DiseaseK23AG034550 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REITZ, CHRISTIANE · 2009 to 2013
$479k
NIA NIH HHS K23 AG034550NIA NIH HHS P01 AG007232NIA NIH HHS P01AG07232NIA NIH HHS P50 AG008702NIA NIH HHS P50 AG08702NIA NIH HHS R01 AG015473NIA NIH HHS R37 AG015473NIA NIH HHS R37AG15473
6 · The paper itself

Abstract

Late-onset Alzheimer's disease (LOAD) is the most common cause of late-onset dementia in western societies. Despite remarkable achievements in human genetics throughout the years, in particular technological advances in gene mapping and in statistical methods that relate genetic variants to disease, to date only a small proportion of the genetic contribution to LOAD can be explained leaving several remaining genetic risk factors to be identified. A possible explanation for the difficulty in gene identification is that LOAD is a multifactorial complex disorder with both genetic and environmental components. Multiple genes with small effects each ("quantitative trait loci"[QTLs]) are likely to contribute to the quantitative traits associated with the disease, such as memory performance, amyloid/tau pathology, or hippocampal atrophy. The motivation for identifying the genetics of LOAD is clear. Not only could it shed light on disease pathogenesis, but it may also provide potential targets for effective treatment, screening, and prevention. Here, we review the usefulness of genetic variation as diagnostic tools and biomarkers in LOAD and discuss the potentials and difficulties researchers face in designing appropriate studies for gene discovery.

Indexed as

Genetic VariationAlzheimer DiseaseBiomarkersHumansPhenotypeBiomarkers

Identifiers

PMID19906263
PMCPMC2819087
OpenAlexW2003137011

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.