Evidence map›Paper›PMID 32592103›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2021

CYP1A2 rs762551 polymorphism and risk for amyotrophic lateral sclerosis.

Vasileios Siokas, Emmanouil Karampinis, Athina-Maria Aloizou, Alexios-Fotios A Mentis, Panagiotis Liakos, Dimitra Papadimitriou, Ioannis Liampas, Grigorios Nasios, Dimitrios P Bogdanos, Georgios M Hadjigeorgiou and 1 more

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Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

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  7. Journal of clinical medicine · 2021
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  8. 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

11 authors at 3 institutions in 2 countries.

Vasileios Siokas *Department of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece.
Emmanouil Karampinis *Department of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece.
Athina-Maria AloizouDepartment of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece.
Alexios-Fotios A MentisDepartment of Microbiology, University of Thessaly, University Hospital of Larissa, Larissa, Greece.
Panagiotis LiakosLaboratory of Biochemistry, Faculty of Medicine, University of Thessaly, Larissa, Greece.
Dimitra PapadimitriouNeurological Department, Henry Dunant Hospital Center, 107 Mesogeion Avenue, 11526, Athens, Greece.
Ioannis LiampasDepartment of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece.
Grigorios NasiosDepartment of Speech and Language Therapy, University of Ioannina, Ioannina, Greece.
Dimitrios P BogdanosDepartment of Rheumatology and Clinical Immunology, University General Hospital of Larissa, Faculty of Medicine, School of Health Sciences, University of Thessaly, Viopolis, 40500, Larissa, Greece.
Georgios M HadjigeorgiouDepartment of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece.
Efthimios DardiotisDepartment of Neurology, Laboratory of Neurogenetics, University of Thessaly, Faculty of Medicine, University Hospital of Larissa, Larissa, Greece. edar@med.uth.gr.ORCID http://orcid.org/0000-0003-2957-641X
University of Thessaly · GRHenry Dunant Hospital · GRUniversity of Ioannina · GR

Funding

The study was supported in part by a research grant of the Research Committee of the University of Thessaly, Greece (Code: 5287). Code: 5287
6 · The paper itself

Abstract

backgroundGenetic variability is considered to confer susceptibility to amyotrophic lateral sclerosis (ALS). Oxidative stress is a significant contributor to ALS-related neurodegeneration, and it is regulated by cytochromes P450 (CYPs), such as CYP1A2; these are responsible for the oxidative metabolism of both exogenous and endogenous substrates in the brain, subsequently impacting ALS. The function of CYP1A2 is largely affected by genetic variability; however, the impact of CYP1A2 polymorphisms in ALS remains underinvestigated.

objectiveThis study aims to examine the possible association of ALS with the CYP1A2 rs762551 polymorphism, which codes for the high inducibility form of the enzyme.

methodsOne hundred and fifty-five patients with sporadic ALS and 155 healthy controls were genotyped for the CYP1A2 rs762551. Statistical testing for the association of CYP1A2 rs762551 with risk for ALS was performed using SNPstats.

resultsThe CYP1A2 rs762551 C allele was associated with a decreased risk of ALS development. In the subgroup analysis according to the ALS site of onset, an association between CYP1A2 rs762551 and limb and bulbar onset of ALS was shown. Cox proportional-hazard regression analyses revealed a significant effect of the CYP1A2 rs762551 on the age of onset of ALS.

conclusionsBased on our results, a primarily potential link between the CYP1A2 rs762551 polymorphism and ALS risk could exist.

Indexed as

Amyotrophic Lateral SclerosisCytochrome P-450 CYP1A2Genetic Predisposition to DiseaseGenotypeHumansPolymorphism, Single NucleotideCYP1A2 protein, humanCytochrome P-450 CYP1A2ALSCYP1A2Oxidative stressPolymorphismrs762551

Identifiers

PMID32592103
OpenAlexW3037001905

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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.