Evidence map›Paper›PMID 26553058›Full record

ArticleNeuromolecular medicine2016

Genetic Factors Affecting Late-Onset Alzheimer's Disease Susceptibility.

Maryam Rezazadeh, Aziz Khorrami, Tarlan Yeghaneh, Mahnaz Talebi, Seyed Jalal Kiani, Yaser Heshmati, Jalal Gharesouran

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Dendrimers: Patents for Alzheimer's Disease.Recent patents on nanotechnology · 2025
    Review
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  5. Review
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  10. Article
  11. Article
  12. Review
  13. Role of Microglia TLRs in Neurodegeneration.Frontiers in cellular neuroscience · 2018
    Article
  14. Article
  15. Review
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

7 authors at 3 institutions in 2 countries.

Maryam RezazadehDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Aziz KhorramiDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Tarlan YeghanehDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahnaz TalebiNeuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyed Jalal KianiVirology Department, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Yaser HeshmatiDepartment of Medicine, Huddinge, H7, Karolinska Institutet, Stockholm, Sweden.
Jalal GharesouranDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Gharesouranj@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IRKarolinska Institutet · SETehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is considered a progressive brain disease in the older population. Late-onset Alzheimer's disease (LOAD) as a multifactorial dementia has a polygenic inheritance. Age, environment, and lifestyle along with a growing number of genetic factors have been reported as risk factors for LOAD. Our aim was to present results of LOAD association studies that have been done in northwestern Iran, and we also explored possible interactions with apolipoprotein E (APOE) status. We re-evaluated the association of these markers in dominant, recessive, and additive models. In all, 160 LOAD and 163 healthy control subjects of Azeri Turkish ethnicity were studied. The Chi-square test with Yates' correction and Fisher's exact test were used for statistical analysis. A Bonferroni-corrected p value, based on the number of statistical tests, was considered significant. Our results confirmed that chemokine receptor type 2 (CCR2), estrogen receptor 1 (ESR1), toll-like receptor 2 (TLR2), tumor necrosis factor alpha (TNF α), APOE, bridging integrator 1 (BIN1), and phosphatidylinositol-binding clathrin assembly protein (PICALM) are LOAD susceptibility loci in Azeri Turk ancestry populations. Among them, variants of CCR2, ESR1, TNF α, and APOE revealed associations in three different genetic models. After adjusting for APOE, the association (both allelic and genotypic) with CCR2, BIN1, and ESRα (PvuII) was evident only among subjects without the APOE ε4, whereas the association with CCR5, without Bonferroni correction, was significant only among subjects carrying the APOE ε4 allele. This result is an evidence of a synergistic and antagonistic effect of APOE on variant associations with LOAD.

Indexed as

Polymorphism, Single NucleotideAdaptor Proteins, Signal TransducingAgedAged, 80 and overAlzheimer DiseaseApolipoprotein E4Apolipoproteins EEstrogen Receptor alphaEthnicityFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansIranLate Onset DisordersAdaptor Proteins, Signal TransducingApoE protein, humanApolipoprotein E4Apolipoproteins EBIN1 protein, humanCCR2 protein, humanESR1 protein, humanEstrogen Receptor alphaMonomeric Clathrin Assembly ProteinsNuclear ProteinsPICALM protein, humanReceptors, CCR2TLR2 protein, humanToll-Like Receptor 2Tumor Necrosis Factor-alphaTumor Suppressor ProteinsAlzheimer’s diseaseAPOEAssociationAzeri TurkishNeurodegenerative diseasesPolymorphism

Identifiers

PMID26553058
OpenAlexW2191737998

What Socratic 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 Socratic graph.