Evidence map›Paper›PMID 21760992›Full record

ArticleInternational journal of Alzheimer's disease2011

Association between the c. 2495 A>G ATP7B Polymorphism and Sporadic Alzheimer's Disease.

Serena Bucossi, Stefania Mariani, Mariacarla Ventriglia, Renato Polimanti, Massimo Gennarelli, Cristian Bonvicini, Patrizio Pasqualetti, Federica Scrascia, Simone Migliore, Fabrizio Vernieri and 2 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of Alzheimer's disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Copper phenotype in Alzheimer's disease: dissecting the pathway.American journal of neurodegenerative disease · 2013
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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 6 institutions in 1 country.

Serena BucossiDepartment of Neurology, Campus Bio-Medico University of Rome, 00128 Rome, Italy.
Stefania Mariani
Mariacarla Ventriglia
Renato Polimanti
Massimo Gennarelli
Cristian Bonvicini
Patrizio Pasqualetti
Federica Scrascia
Simone Migliore
Fabrizio Vernieri
Paolo M Rossini
Rosanna Squitti
Fatebenefratelli Hospital · ITUniversità Campus Bio-Medico · ITCentro San Giovanni di Dio Fatebenefratelli · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversità degli studi di Cassino e del Lazio Meridionale · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonceruloplasmin-bound copper ("free") is reported to be elevated in Alzheimer's disease (AD). In Wilson's disease (WD) Cu-ATPase 7B protein tightly controls free copper body levels. To explore whether the ATP7B gene harbours susceptibility loci for AD, we screened 180 AD chromosomes for sequence changes in exons 2, 5, 8, 10, 14, and 16, where most of the Mediterranean WD-causing mutations lie. No WD mutation, but sequence changes corresponding to c.1216 T>G Single-Nucleotide Polymorphism (SNP) and c.2495 A>G SNP were found. Thereafter, we genotyped 190 AD patients and 164 controls for these SNPs frequencies estimation. Logistic regression analyses revealed either a trend for the c.1216 SNP (P = .074) or a higher frequency for c.2495 SNP of the GG genotype in patients, increasing the probability of AD by 74% (P = .028). Presence of the GG genotype in ATP7B c.2495 could account for copper dysfunction in AD which has been shown to raise the probability of the disease.

Identifiers

PMID21760992
PMCPMC3132548
OpenAlexW2021962286

What OpenQuestion holds

Textmetadata
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.