Searching for the role and the most suitable biomarkers of oxidative stress in Alzheimer's disease and in other neurodegenerative diseases

Migliore, Lucia; Fontana, Ilaria; Colognato, Renato; Coppedè, Fabio; Siciliano, Gabriele; Murri, Luigi

doi:10.1016/j.neurobiolaging.2004.10.002

Cited by 121 publications

(57 citation statements)

References 91 publications

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“…The nervous system is particularly sensitive to damage caused by oxidative stress due to its high oxygen uptake rate, high polyunsaturated fatty acids rate, and relatively low antioxidant defense degree when compared to other tissues [12]. Moreover, the structures observed in AD, namely β-amyloid plaques and neuroﬁbrillary tangles, are associated with oxidative stress, since some studies have shown that they induce lipid peroxidation and cell apoptosis [10,13,14]. Thus, the role of glutathione peroxidases (GPx) may be considered very important, as this family of selenium (Se)-dependent enzymes catalyzes the reduction of hydrogen peroxide, organic hydroperoxide, and lipid peroxides by reducing glutathione and then protects cells against oxidative damage [15].…”

Section: Introductionmentioning

confidence: 99%

Glutathione Peroxidase 1 Pro198Leu Polymorphism in Brazilian Alzheimer’s Disease Patients: Relations to the Enzyme Activity and to Selenium Status

et al. 2012

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Background/Aims: Oxidative stress plays a central role in Alzheimer’s disease (AD). Pro198Leu cytosolic glutathione peroxidase (GPx1) polymorphism seems to be associated with a lower activity of this enzyme, but there are no studies with AD patients. Thus, the aim was to determine the frequency of the GPx1 Pro198Leu polymorphism in AD patients and to verify its relation to glutathione peroxidase (GPx) activity and selenium (Se) status. Methods: The study was carried out in a group of AD elderly (n = 28) compared to a control group (n = 29). Blood Se concentrations were measured through hydride generation atomic absorption spectroscopy. GPx activity was determined using a commercial kit, and the polymorphism using amplified DNA sequencing. Results: The distribution of genotypes was not different between groups. The variant allele frequency was 0.179 (AD group) and 0.207 (control group). Although no differences regarding GPx activity were found between individuals with different genotypes, lower blood Se levels were found in Pro/Pro AD patients compared to Pro/Pro control subjects, which was not found in the Pro/Leu groups. Moreover, the association between the erythrocyte Se concentration and GPx activity was affected by the Pro198Leu genotype. Conclusions: Results indicate that this polymorphism had apparently affected Se status in AD patients and that more studies in this field are necessary.

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Section: Introductionmentioning

confidence: 99%

Glutathione Peroxidase 1 Pro198Leu Polymorphism in Brazilian Alzheimer’s Disease Patients: Relations to the Enzyme Activity and to Selenium Status

et al. 2012

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“…[36][37][38][39] Studies related to the role of oxidative stress in neurodegenerative diseases are limited with patients with AD and several studies demonstrated elevated levels of oxidative DNA damage and an impairment in the removal of oxidized purines in the lymphocytes of patients with AD. [16][17][18][19] A significant increase of 8OHG and an oxidized amino acid (nitrotyrosine) were detected in neurons of patients with AD suggesting that increased oxidative damage is an early event in AD that decreases with the progression of the disease. 40 The level of oxidative damage and repair capacity in peripheral lymphocytes of AD patients and their age-matched controls was determined by the comet assay applied to freshly isolated blood samples with oxidative lesion-specific DNA repair endonucleases.…”

Section: Discussionmentioning

confidence: 99%

“…Increased levels of redox active iron and lipid peroxidation, increased RNA oxidation and nuclear DNA oxidation, increased mitochondrial oxidation, decreased level of neural polyunsaturated fatty acid and protein oxidation have been demonstrated in patients with AD. [11][12][13][14][15][16] A significantly higher levels of basal and oxidative DNA damage were found in the lymphocytes as well as in the polymorphonuclear leukocytes of patients with AD and with mild cognitive impairment (MCI). [17][18][19] Studies in patients with AD showed increased levels of 8-hydroxyguanosine (8OHG) or 8-hydroxy-2'-deoxyguanosine (8OHdG) in addition to decreased levels of plasma antioxidants as compared to controls.…”

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confidence: 99%

Assessment of DNA Damage in the Peripheral Lymphocytes of Patients with Parkinson's Disease and Multiple Sclerosis Using the Comet Assay

Baydar¹,

Aydın²,

Ündeğer³

et al. 2013

Turkiye Klinikleri J Med Sci

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A AB BS ST TR RA AC CT T O Ob bj je ec ct ti iv ve e: : It has been suggested that oxidative damage have been involved in the pathogenesis of neurodegenerative diseases. Although the role of oxidative stress in the etiology of these diseases is not clear, the increased levels of DNA damage and protein as well as DNA and mitochondrial oxidation have been demonstrated in patients with Parkinson's disease (PD) and Alzheimer's disease (AD) in a few studies. M Ma at te er ri ia al l a an nd d M Me et th ho od ds s: : In this study, the levels of DNA damage in the peripheral lymphocytes of patients with PD and multiple sclerosis (MS), and their age-matched healthy controls were determined by the comet assay with and without treatment of blood samples with 50μM hydrogen peroxide (H2O2) and the oxidative purine specific DNA repair enzyme, formamidopyrimidine glycosylase (Fpg). R Re es su ul lt ts s: : The DNA damage in the lymphocytes of the patients with PD has been significantly increased compared to controls. However, no significant increase in the DNA strand breakage was detected in the patients with PD after treatment with either H2O2 or Fpg. Although the DNA damage in the MS patients was higher than their healthy controls, the difference was not found to be significant. A significant increase observed in the DNA damage after treatment with H2O2 and with Fpg in MS patients, have suggested the susceptibility to oxidative DNA damage in these patients. C Co on nc cl lu us si io on n: : The data presented in this paper shows high level of DNA damage in the lymphocytes of patients with PD and MS which indicates the possibility of oxidative stres in these neurodegenerative diseases.

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“…Although AD is a disease of central nervous system, peripheral manifestations have been observed in patients with MCI and AD. In the process of neurodegeneration, a variety of macromolecules seem to be damaged [147]. There are two hypotheses for peripheral oxidative stress leading to neurodegeneration.…”

Section: Oxidative Stress Markersmentioning

confidence: 99%

Genetic and Blood Biomarkers of Alzheimer`s Disease

Momeni¹,

Ferrari²

2010

TONMEDJ

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Alzheimer's disease (AD) is the most prevalent form of dementia. AD is highly heritable, with a complex pattern. Although clinical diagnosis is based on accurate and well defined diagnostic criteria (NINCDS-ADRDA), the definite diagnosis relies on the postmortem pathological findings. The need for measures for the early detection of AD, as well as the need to distinguish between AD and other forms of dementia, has put great emphasis on the discovery of biomarkers for Alzheimer's disease. In clinical practice, there is need for non-invasive, accurate methods for the early detection and differential diagnosis of AD. The successful identification and development of the biomarkers, depends completely on the understanding of pathology, genetic and molecular mechanisms involved in the disease. As blood is a circulating dynamic tissue and transcription reflects the ongoing changes in the system, it makes the transcriptional profiling of the blood cells, potentially, the most sensitive source for transcriptional biomarkers. A systematic comparison of the genetic and proteomic blood biomarkers in patients and healthy controls can reveal additional potential candidates for AD. In the first part of this review, we would like to discuss the most recent genetic findings and their possible involvement in the pathogenesis of AD. In the second part, we review the blood biomarkers which can be derived from peripheral blood mononuclear cells (PBMC), serum, and plasma. We discus three main category of bio-molecules, namely DNA, RNA (miRNA and mRNA), and protein as well as their possible role in the hypothetical mechanisms involved in pathogenesis of AD. A dynamic interaction between the genetic findings through the whole genome association studies and biomarkers discovery can advance our knowledge of AD pathogenesis beyond the scope of each field independently.

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Searching for the role and the most suitable biomarkers of oxidative stress in Alzheimer's disease and in other neurodegenerative diseases

Cited by 121 publications

References 91 publications

Glutathione Peroxidase 1 Pro198Leu Polymorphism in Brazilian Alzheimer’s Disease Patients: Relations to the Enzyme Activity and to Selenium Status

Glutathione Peroxidase 1 Pro198Leu Polymorphism in Brazilian Alzheimer’s Disease Patients: Relations to the Enzyme Activity and to Selenium Status

Assessment of DNA Damage in the Peripheral Lymphocytes of Patients with Parkinson's Disease and Multiple Sclerosis Using the Comet Assay

Genetic and Blood Biomarkers of Alzheimer`s Disease

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