Association between single nucleotide polymorphisms of MUTYH, hOGG1 and NEIL1 genes, and depression

Czarny, Piotr; Kwiatkowski, Dominik; Gałecki, Piotr; Talarowska, Monika; Orzechowska, Agata; Bobińska, Kinga; Bielecka-Kowalska, Anna; Szemraj, Janusz; Maes, Michaël; Su, Kuan‐Pin; Śliwiński, Tomasz

doi:10.1016/j.jad.2015.05.044

Cited by 32 publications

(22 citation statements)

References 36 publications

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“…The same group further genotyped single nucleotide polymorphisms (SNPs) of three genes encoding glycosylases, which are essential enzymes for adequate operation of base excision repair (BER). They found a stronger association of certain SNPs with early-onset depression than with late-onset depression supporting the hypothesis that altered DNA repair may be involved in pathogenesis of depression (Czarny et al 2015a). Other studies also showed an increased level of telomere shortening (Simon et al 2006) and an increased frequency of DNA damage (Andreazza et al 2007).…”

Section: Dna Damage In Mddmentioning

confidence: 62%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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Human cells are exposed to exogenous insults and continuous production of different metabolites. These insults and unwanted metabolic products might interfere with the stability of genomic DNA. Recently many studies demonstrated that different psychiatric disorders show substantially high level of oxidative DNA damage in the brain accompanied with morphological and functional alterations. It reveals that damaged genomic DNA may contribute to the pathophysiology of these mental illnesses. Here we review the role of oxidative damage and reduced antioxidant ability in some vastly studied psychiatric disorders and emphasize the inclusion of treatment options involving DNA repair. In addition, while most currently used antidepressants are based on the manipulation of the neurotransmitter regulation in managing different mental abnormalities, they are able to prevent or reverse neurotoxin-induced DNA damage. Therefore, it may be plausible to target on genomic DNA alterations for psychiatric therapies, which is of pivotal importance for future anti-psychiatric drug development.

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Section: Dna Damage In Mddmentioning

confidence: 62%

DNA Damage in Major Psychiatric Diseases

et al. 2016

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“…Similar results were obtained in studies on depression. It was found that the combined genotypes C/C×C/C of c.977C>G (hOGG1) and c.*589G>C (NEIL1) significantly reduce the risk of recurrent depressive disorder [59]. …”

Section: Discussionmentioning

confidence: 99%

Association between Single-Nucleotide Polymorphisms of the hOGG1,NEIL1,APEX1, FEN1,LIG1, and LIG3 Genes and Alzheimer's Disease Risk

Kwiatkowski

Czarny²,

Toma³

et al. 2016

Neuropsychobiology

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Background: One of the factors that contribute to Alzheimer's disease (AD) is the DNA damage caused by oxidative stress and inflammation that occurs in nerve cells. It has been suggested that the risk of AD may be associated with an age-dependent reduction of the DNA repair efficiency. Base excision repair (BER) is, among other things, a main repair system of oxidative DNA damage. One of the reasons for the reduced efficiency of this system may be single-nucleotide polymorphisms (SNP) of the genes encoding its proteins. Methods: DNA for genotyping was obtained from the peripheral blood of 281 patients and 150 controls. In the present study, we evaluated the impact of 8 polymorphisms of 6 BER genes on the AD risk. We analyzed the following SNP: c.-468T>G and c.444T>G of APEX1, c.*50C>T and c.*83A>C of LIG3, c.977C>G of OGG1, c.*283C>G of NEIL1, c.-441G>A of FEN1, and c.-7C>T of LIG1. Results: We showed that the LIG1 c.-7C>T A/A and LIG3 c.*83A>C A/C variants increased, while the APEX1 c.444T>G G/T, LIG1 c.-7C>T G/, LIG3 c.*83A>C C/C variants reduced, the AD risk. We also evaluated the relation between gene-gene interactions and the AD risk. We showed that combinations of certain BER gene variants such as c.977C>G×c.*50C>T CC/CT, c.444T>G×c.*50C>T GG/CT, c.-468T>G×c.*50C>T GG/CT, c.-441G>Ac.*50C>T×c.*50C>T GG/CT, c.*83A>C× c.*50C>T CT/AC, and c.-7C>T×c.*50C>T CT/GG can substantially positively modulate the risk of AD. Conclusions: In conclusion, we revealed that polymorphisms of BER genes may have a significant effect on the AD risk, and the presence of polymorphic variants may be an important marker for AD.

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“…One of the factors that may cause defective DNA damage repair is the presence of specific polymorphic variants of genes encoding proteins involved in this repair [18, 19]. Therefore, we genotyped 12 SNPs of BER genes in a larger group consisting of more than 550 participants and found that some of them can modulate rDD risk [17]. …”

Section: Discussionmentioning

confidence: 99%

“…Our previous study utilizing comet assay technique on the PBMCs of patients diagnosed with clinical depression confirmed the presence of not only oxidatively modified purines and pyrimidines but also other types of DNA damage, like DNA strand breaks [16]. Furthermore, we also noted that increased DNA damage in patients with depression might be caused not only by the disease itself but also by the impairments of oxidative DNA damage repair, since we observed that the patients’ cells repaired DNA damage induced by hydrogen peroxide (H 2 O 2 ) more slowly than the controls’ cells [17]. Since it was shown that single nucleotide polymorphism (SNP) variants of genes involved in DDR, particularly BER, may negatively affect the process, we genotyped the SNPs of genes involved in this repair pathway [16–18].…”

Section: Introductionmentioning

confidence: 97%

Impact of Single Nucleotide Polymorphisms of Base Excision Repair Genes on DNA Damage and Efficiency of DNA Repair in Recurrent Depression Disorder

et al. 2016

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Elevated level of DNA damage was observed in patients with depression. Furthermore, single nucleotide polymorphisms (SNPs) of base excision repair (BER) genes may modulate the risk of this disease. Therefore, the aim of this study was to delineate the association between DNA damage, DNA repair, the presence of polymorphic variants of BER genes, and occurrence of depression. The study was conducted on peripheral blood mononuclear cells of 43 patients diagnosed with depression and 59 controls without mental disorders. Comet assay was used to assess endogenous (oxidative) DNA damage and efficiency of DNA damage repair (DRE). TaqMan probes were employed to genotype 12 SNPs of BER genes. Endogenous DNA damage was higher in the patients than in the controls, but none of the SNPs affected its levels. DRE was significantly higher in the controls and was modulated by BER SNPs, particularly by c.977C>G–hOGG1, c.972G>C–MUTYH, c.2285T>C–PARP1, c.580C>T–XRCC1, c.1196A>G–XRCC1, c.444T>G–APEX1, c.-468T>G–APEX1, or c.*50C>T–LIG3. Our study suggests that both oxidative stress and disorders in DNA damage repair mechanisms contribute to elevated levels of DNA lesions observed in depression. Lower DRE can be partly attributed to the presence of specific SNP variants.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-016-9971-6) contains supplementary material, which is available to authorized users.

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Association between single nucleotide polymorphisms of MUTYH, hOGG1 and NEIL1 genes, and depression

Cited by 32 publications

References 36 publications

DNA Damage in Major Psychiatric Diseases

DNA Damage in Major Psychiatric Diseases

Association between Single-Nucleotide Polymorphisms of the <b><i>hOGG1,</i></b><b><i>NEIL1,</i></b><b><i>APEX1, FEN1,</i></b><b><i>LIG1,</i></b> and <b><i>LIG3</i></b> Genes and Alzheimer's Disease Risk

Impact of Single Nucleotide Polymorphisms of Base Excision Repair Genes on DNA Damage and Efficiency of DNA Repair in Recurrent Depression Disorder

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