Expression and Polymorphisms of Gene 8-Oxoguanine Glycosylase 1 and the Level of Oxidative DNA Damage in Peripheral Blood Lymphocytes of Patients with Alzheimer's Disease

Dorszewska, Jolanta; Kempisty, Bartosz; Jaroszewska-Kolecka, Joanna; Różycka, Agata; Florczak, Jolanta; Lianeri, Margarita; Jagodzińśki, Paweł P.; Kozubski, Wojciech

doi:10.1089/dna.2009.0926

Cited by 48 publications

(41 citation statements)

References 48 publications

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“…MTH1 possesses the specific enzymatic activity necessary to convert the deleterious 8-oxoguanine-containing deoxyribonucleoside triphosphate into monophosphates, thus preventing its misincorporation into DNA and thereby minimizing the accumulation of oxidized DNA in neurons. Additionally, MTH1 activity is significantly decreased in AD subjects (28,29). Therefore, we examined the effect of MTH1 on estrogen-mediated DNA protection.…”

Section: Discussionmentioning

confidence: 97%

Phytoestrogen α-zearalanol ameliorates memory impairment and neuronal DNA oxidation in ovariectomized mice

Dong¹,

Wang²,

Liu³

et al. 2013

Clinics

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OBJECTIVE:The aim of this study was to evaluate the effect of a novel phytoestrogen, α-Zearalanol, on Alzheimer's disease-related memory impairment and neuronal oxidation in ovariectomized mice.METHODS:Female C57/BL6 mice were ovariectomized or received sham operations and treatment with equivalent doses of 17β-estradiol or α-Zearalanol for 8 weeks. Their spatial learning and memory were analyzed using the Morris water maze test. The antioxidant enzyme activities and reactive oxygen species generation, neuronal DNA oxidation, and MutT homolog 1 expression in the hippocampus were measured.RESULTS:Treatment with 17β-estradiol or α-Zearalanol significantly improved spatial learning and memory performance in ovariectomized mice. In addition, 17β-estradiol and α-Zearalanol attenuated the decrease in antioxidant enzyme activities and increased reactive oxygen species production in ovariectomized mice. The findings indicated a significant elevation in hippocampi neuronal DNA oxidation and reduction in MutT homolog 1 expression in estrogen-deficient mice, but supplementation with 17β-estradiol or α-Zearalanol efficaciously ameliorated this situation.CONCLUSION:These results demonstrate that α-Zearalanol is potentially beneficial for improving memory impairments and neuronal oxidation damage in a manner similar to that of 17β-estradiol. Therefore, the compound may be a potential therapeutic agent that can ameliorate neurodegenerative disorders related to estrogen deficiency.

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Section: Discussionmentioning

confidence: 97%

Phytoestrogen α-zearalanol ameliorates memory impairment and neuronal DNA oxidation in ovariectomized mice

Dong¹,

Wang²,

Liu³

et al. 2013

Clinics

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“…In this study, we focused on the variants of the OGG1 gene that had previously been investigated for breast cancer, bladder cancer, and Alzheimer's disease [24][25][26]. We found a statistically significant association between the RA and the rs3219008 polymorphism.…”

Section: Discussionmentioning

confidence: 99%

Association of the C-285T and A5954G polymorphisms in the DNA repair gene OGG1 with the susceptibility of rheumatoid arthritis

et al. 2011

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Rheumatoid arthritis (RA) is a chronic autoimmune disease and can lead to deformities and severe disabilities, due to irreversible damage of tendons, joints, and bones. Previous study indicated that DNA repair system was involved in the pathology of RA. In this study, we investigated the association of two 8-oxoguanine glycosylase 1 (OGG1) gene polymorphisms (rs159153 and rs3219008) with the susceptibility to RA in 384 Taiwanese individuals (192 patients with RA and 192 controls). Our data showed that statistically significant difference in genotype frequency distributions was found at rs3219008 SNP between patients with RA and control groups (P = 5.6E-0.5). Our data also indicated that individuals with the AG genotype at rs3219008 SNP may have a higher risk of developing RA. We did not observe any statistically significant association of OGG1 haplotype frequencies (rs159153 and rs3219008) with RA progression. The study suggested that OGG1 polymorphisms (rs159153 and rs3219008) are associated with RA progression and that these may be used as molecular markers of RA.

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“…Studies found no significant associations between the Ser326Cys polymorphism in OGG1 and AD (Coppede et al, 2007; Dorszewska et al, 2009; Parildar-Karpuzoglu et al, 2008), although there are some reports on OGG1 mutations (A53T and A288V) in AD patients (Jacob et al, 2013; Mao et al, 2007). MUTYH, an adenine DNA glycosylase that removes adenine opposite 8-oxodG base pairs (Oka and Nakabeppu, 2011), has also been evaluated and no significant associations between MUTYH and late-onset AD risk identified (Kwiatkowski et al, 2015).…”

Section: Polymorphisms Of Dna Repair Genes In Alzheimer’s Diseasementioning

confidence: 94%

Genome instability in Alzheimer disease

Song

Croteau

et al. 2017

Mechanisms of Ageing and Development

101

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia. Autosomal dominant, familial AD (fAD) is very rare and caused by mutations in amyloid precursor protein (APP), presenilin-1 (PSEN-1), and presenilin-2 (PSEN-2) genes. The pathogenesis of sporadic AD (sAD) is more complex and variants of several genes are associated with an increased lifetime risk of AD. Nuclear and mitochondrial DNA integrity is pivotal during neuronal development, maintenance and function. DNA damage and alterations in cellular DNA repair capacity have been implicated in the aging process and in age-associated neurodegenerative diseases, including AD. These findings are supported by research using animal models of AD and in DNA repair deficient animal models. In recent years, novel mechanisms linking DNA damage to neuronal dysfunction have been identified and have led to the development of noninvasive treatment strategies. Further investigations into the molecular mechanisms connecting DNA damage to AD pathology may help to develop novel treatment strategies for this debilitating disease. Here we provide an overview of the role of genome instability and DNA repair deficiency in AD pathology and discuss research strategies that include genome instability as a component

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Expression and Polymorphisms of Gene 8-Oxoguanine Glycosylase 1 and the Level of Oxidative DNA Damage in Peripheral Blood Lymphocytes of Patients with Alzheimer's Disease

Cited by 48 publications

References 48 publications

Phytoestrogen α-zearalanol ameliorates memory impairment and neuronal DNA oxidation in ovariectomized mice

Phytoestrogen α-zearalanol ameliorates memory impairment and neuronal DNA oxidation in ovariectomized mice

Association of the C-285T and A5954G polymorphisms in the DNA repair gene OGG1 with the susceptibility of rheumatoid arthritis

Genome instability in Alzheimer disease

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