Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer’s disease

Previous studies have provided evidence of the involvement of oxidative damage in the pathogenesis of Alzheimer’s disease (AD). Although the role of oxidative stress in the aetiology of the disease is still not clear, the detection of an increased damage status in the cells of patients could have im...

Full description

Saved in:
Bibliographic Details
Published inNeurobiology of aging Vol. 23; no. 1; pp. 47 - 53
Main Authors Mórocz, Mónika, Kálmán, János, Juhász, Anna, Sinkó, Ildikó, McGlynn, Angela P, Downes, C.Stephen, Janka, Zoltán, Raskó, István
Format Journal Article
LanguageEnglish
Published London Elsevier Inc 2002
Elsevier Science
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Previous studies have provided evidence of the involvement of oxidative damage in the pathogenesis of Alzheimer’s disease (AD). Although the role of oxidative stress in the aetiology of the disease is still not clear, the detection of an increased damage status in the cells of patients could have important therapeutic implications. The level of oxidative damage and repair capacity in peripheral lymphocytes of AD patients and of age-matched controls was determined by the Comet assay applied to freshly isolated blood samples with oxidative lesion-specific DNA repair endonucleases. This is less prone to errors arising from oxidative artifacts than chemical analytical methods; and is therefore a relatively reliable, as well as rapid method for assay of oxidative DNA damage in cells. Statistically significant elevations ( P < 0.05) of oxidized purines were observed in nuclear DNA of peripheral lymphocytes from AD patients, compared to age matched control subjects, both at basal level and after oxidative stress induced by H 2O 2. AD patients also showed a diminished repair of H 2O 2 -induced oxidized purines.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-News-3
ISSN:0197-4580
1558-1497
DOI:10.1016/S0197-4580(01)00257-3