SynthesisBMC medical genetics2014
Genetic associations of Nrf2-encoding NFE2L2 variants with Parkinson's disease - a multicenter study.
Synthesis in BMC medical genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- The DJ1-Nrf2-STING axis mediates the neuroprotective effects of Withaferin A in Parkinson's disease.Cell death and differentiation · 2021Pooled it
- Brain B Vitamin Status and One-Carbon Metabolism Gene Polymorphisms are Associated with Cognitive Impairment in Alzheimer's and Parkinson's Disease.bioRxiv : the preprint server for biology · 2026Article
- Targeting the bile acid receptor TGR5 with Gentiopicroside to activate Nrf2 antioxidant signaling and mitigate Parkinson's disease in an MPTP mouse model.Journal of advanced research · 2026Article
- Health position paper and redox perspectives - Bench to bedside transition for pharmacological regulation of NRF2 in noncommunicable diseases.Redox biology · 2025Review
- Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.Redox biology · 2025Review
- Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.Biomolecules · 2025Review
- Interplay of oxidative stress and Inflammasome activation and clinical indices in Parkinson's disease: insights from serum SIRT1, Nrf2, and NLRP3 levels and PDQ-39-a cross-sectional study.Frontiers in neuroscience · 2025Article
- Gardenin A treatment attenuates inflammatory markers, synuclein pathology and deficits in tyrosine hydroxylase expression and improves cognitive and motor function in A53T-α-syn mice.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Interactions Between the Ubiquitin-Proteasome System, Nrf2, and the Cannabinoidome as Protective Strategies to Combat Neurodegeneration: Review on Experimental Evidence.Neurotoxicity research · 2024Review
- Association of NEF2L2 Rs35652124 Polymorphism with Nrf2 Induction and Genotoxic Stress Biomarkers in Autism.Genes · 2023Article
- Quantitative and causal analysis for inflammatory genes and the risk of Parkinson's disease.Frontiers in immunology · 2023Article
- Nrf2/Keap1/ARE signaling: Towards specific regulation.Life sciences · 2022Review
- Novel Series of Dual NRF2 Inducers and Selective MAO-B Inhibitors for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2022Article
- Nrf2 rs6721961 and Oxidative Stress in Preeclampsia: Association with the Risk of Preeclampsia and Early-Onset Preeclampsia.International journal of molecular and cellular medicine · 2022Article
- Nrf2 as a potential target for Parkinson's disease therapy.Journal of molecular medicine (Berlin, Germany) · 2021Review
- SNPs in miRNAs and Target Sequences: Role in Cancer and Diabetes.Frontiers in genetics · 2021Review
- Peripheral Blood NRF2 Expression as a Biomarker in Human Health and Disease.Antioxidants (Basel, Switzerland) · 2020Article
- Review
- Environmental risk factors and their footprints in vivo - A proposal for the classification of oxidative stress biomarkers.Redox biology · 2020Review
- A Systematic Analysis Revealed the Potential Gene Regulatory Processes of ATRA-Triggered Neuroblastoma Differentiation and Identified a Novel RA Response Sequence in theBioMed research international · 2020Article
Corrections and comments
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Authors and funding
15 authors at 11 institutions in 7 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transcription factor Nrf2, encoded by the NFE2L2 gene, is an important regulator of the cellular protection against oxidative stress. Parkinson's disease is a neurodegenerative disease highly associated with oxidative stress. In a previously published study, we reported associations of NFE2L2 haplotypes with risk and age at onset of idiopathic Parkinson's disease in a Swedish discovery material and a Polish replication material. Here, we have extended the replication study and performed meta-analyses including the Polish material and four new independent European patient-control materials. Furthermore, all SNPs included in the haplotype windows were investigated individually for associations with Parkinson's disease in meta-analyses including all six materials.
methodsTotally 1038 patients and 1600 control subjects were studied. Based on previous NFE2L2 haplotype associations with Parkinson's disease, five NFE2L2 tag SNPs were genotyped by allelic discrimination and three functional NFE2L2 promoter SNPs were genotyped by sequencing. The impact of individual SNPs and haplotypes on risk and age at onset of Parkinson's disease were investigated in each material individually and in meta-analyses of the obtained results.
resultsMeta-analyses of NFE2L2 haplotypes showed association of haplotype GAGCAAAA, including the fully functional promoter haplotype AGC, with decreased risk (OR = 0.8 per allele, p = 0.012) and delayed onset (+1.1 years per allele, p = 0.048) of Parkinson's disease. These results support the previously observed protective effect of this haplotype in the first study. Further, meta-analyses of the SNPs included in the haplotypes revealed four NFE2L2 SNPs associated with age at onset of Parkinson's disease (rs7557529 G > A, -1.0 years per allele, p = 0.042; rs35652124 A > G, -1.1 years per allele, p = 0.045; rs2886161 A > G, -1.2 years per allele, p = 0.021; rs1806649 G > A, +1.2 years per allele, p = 0.029). One of these (rs35652124) is a functional SNP located in the NFE2L2 promoter. No individual SNP was associated with risk of Parkinson's disease.
conclusionOur results support the hypothesis that variation in the NFE2L2 gene, encoding a central protein in the cellular protection against oxidative stress, may contribute to the pathogenesis of Parkinson's disease. Functional studies are now needed to explore these results further.
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