Evidence map›Paper›PMID 21899770›Full record

ArticleBMC research notes2011

Genetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease risk.

José L Vázquez-Higuera, Ignacio Mateo, Pascual Sánchez-Juan, Eloy Rodríguez-Rodríguez, Ana Pozueta, Miguel Calero, José L Dobato, Ana Frank-García, Fernando Valdivieso, José Berciano and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. The crystal structure of the catalytic domain of tau tubulin kinase 2 in complex with a small-molecule inhibitor.Acta crystallographica. Section F, Structural biology communications · 2020
    Article
  7. Article
  8. Cracking the ANP32 whips: important functions, unequal requirement, and hints at disease implications.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014
    Article
  9. Review
  10. 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

12 authors at 7 institutions in 1 country.

José L Vázquez-HigueraNeurology Service and CIBERNED, "Marqués de Valdecilla" University Hospital (University of Cantabria and IFIMAV), Santander, Spain. combarro@unican.es.
Ignacio Mateo
Pascual Sánchez-Juan
Eloy Rodríguez-Rodríguez
Ana Pozueta
Miguel Calero
José L Dobato
Ana Frank-García
Fernando Valdivieso
José Berciano
Maria J Bullido
Onofre Combarros
Centro de Investigación Biomédica en Red · ESMarqués de Valdecilla University Hospital · ESUniversidad de Cantabria · ESCentro de Biología Molecular Severo Ochoa · ESFundacion Centro De Investigacion De Enfermedades Neurologicas · ESHospital Universitario La Paz · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTau abnormal hyperphosphorylation and the formation of neurofibrillary tangles in AD brain is the result of upregulation of tau kinases and downregulation of tau phosphatases.

methodsIn a group of 729 Spanish late-onset Alzheimer's disease (AD) patients and 670 healthy controls, we examined variations into a set of candidate genes (PPP2CA, PPP2R2A, ANP32A, LCMT1, PPME1 and PIN1) in the tau protein phosphatase-2A (PP2A) pathway, to address hypotheses of genetic variation that might influence AD risk.

resultsThere were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by age, gender or APOE ε4 allele.

conclusionOur negative findings in the Spanish population argue against the hypothesis that genetic variation in the tau protein phosphatase-2A (PP2A) pathway is causally related to AD risk.

Identifiers

PMID21899770
PMCPMC3224542
OpenAlexW1972956891

What OpenQuestion holds

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Registered trials

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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.