Evidence map›Paper›PMID 23036585›Full record

ArticleNeurobiology of aging2013

Exploratory analysis of seven Alzheimer's disease genes: disease progression.

Agustín Ruiz, Isabel Hernández, Maiteé Ronsende-Roca, Antonio González-Pérez, Emma Rodriguez-Noriega, Reposo Ramírez-Lorca, Ana Mauleón, Concha Moreno-Rey, Lucie Boswell, Larry Tune and 13 more

Erratum issuedAbstract read
In one paragraph

Article in Neurobiology of aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Observational
  7. The Role of PICALM in Alzheimer's Disease.Molecular neurobiology · 2015
    Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

23 authors.

Agustín RuizMemory Clinic of Fundació ACE, Institut Català de Neurociències Aplicades, Barcelona, Spain. aruiz@fundacioace.com
Isabel Hernández
Maiteé Ronsende-Roca
Antonio González-Pérez
Emma Rodriguez-Noriega
Reposo Ramírez-Lorca
Ana Mauleón
Concha Moreno-Rey
Lucie Boswell
Larry Tune
Sergi Valero
Montserrat Alegret
Javier Gayán
James T Becker
Luis Miguel Real
Lluís Tárraga
Clive Ballard
Michael Terrin
Stephanie Sherman
Haydeh Payami
Oscar L López
Jacobo E Mintzer
Mercè Boada

Funding

TREATMENT OF DEPRESSION IN ALZHEIMER'S DISEASEP50AG005133 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECKER, JAMES T. · 1985 to 2019
$43.0M
NIA NIH HHS P50 AG005133
6 · The paper itself

Abstract

The relationships between genome wide association study-identified and replicated genetic variants associated with Alzheimer's disease (AD) risk and disease progression or therapeutic responses in AD patients are almost unexplored. Seven hundred and one AD patients with at least 3 different cognitive evaluations and genotypic information for APOE and 6 genome wide association study-significant single-nucleotide polymorphisms were selected for this study. Mean differences in Global Deterioration Score and Mini Mental State Examination (MMSE) were evaluated using nonparametric tests, general linear model and mixed models for repeated measurements. Each chart was also reviewed for evidence of treatment with any cholinesterase inhibitor, memantine, or both. Relationships between therapeutic protocols, genetic markers, and progression were explored using stratified analysis looking for specific effects on progression in each therapeutic category separately. Neither calculation rendered a Bonferroni-corrected statistically significant difference in any genetic marker. Mixed model results suggested differences in the average point in MMSE test for patients carrying PICALM GA or AA genotype compared with GG carriers at the end of the follow-up (MMSE mean difference = -0.57; 95% confidence interval, -1.145 to 0.009; p = 0.047). This observation remained unaltered after covariate adjustments although it did not achieve predefined multiple testing significance threshold. The PICALM single-nucleotide polymorphism also displayed a significant effect protecting against rapid progression during pharmacogenetic assays although its observed effect displayed heterogeneity among AD therapeutic protocols (p = 0.039). None of the studied genetic markers were convincingly linked to AD progression or drug response. However, by using different statistical approaches, the PICALM rs3851179 marker displayed consistent but weak effects on disease progression phenotypes.

Indexed as

Disease ProgressionAgedAged, 80 and overAlzheimer DiseaseFemaleGenetic Association StudiesGenetic MarkersGenetic Predisposition to DiseaseHumansMalePolymorphism, Single NucleotidePrevalenceRisk FactorsSpainGenetic Markers

Identifiers

PMID23036585
PMCPMC4097044

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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.