2024-03-28T17:44:35Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1220242016-02-18T03:25:42Zcom_10261_42343com_10261_2col_10261_42344
2015-09-14T09:57:30Z
urn:hdl:10261/122024
Study of plasma antioxidant status in Alzheimer's disease
Pulido, R.
Jiménez Escrig, Antonio
Orensanz, L.
Saura Calixto, Fulgencio D.
To examine the plasma antioxidant status of Alzheimer's disease (AD) patients and to evaluate the influence of apolipoprotein E (APOE) genotype. There are reasons to suspect involvement of the free hydroxyl radical in the pathogenesis of AD. In contrast, studies in plasma of AD patients for the evaluation of levels of biomarkers of oxidation are controversial. Twenty AD patients diagnosed using the National Institute for Neurological Disorders/Alzheimer's Disease and Related Disorders (NINDS/ADRDA) criteria and 22 controls chosen amongst different subjects without cognitive damage. All the subjects - both AD patients and controls - were stratified by their APOE genotype (3/3, 3/4 or 4/4), which was determined by PCR. Plasma total antioxidant capacity (TAC) was determined using two complementary procedures: FRAP, which measures the ferric reduction capacity, and ABTS, which measures the radical scavenging capacity. In addition, 2-amino-adipic semialdehyde (2-AAS), a biomarker of protein oxidation, was evaluated. No significant difference was observed between the AD and control groups regarding plasma TAC. When the subjects were classified by their APOE genotype, significant differences were found in the APOE 4/4 group in the TCA determined by the FRAP method. Subjects with APOE genotype 4/4, which is the group with higher incidence in AD, showed lower antioxidant capacity of plasma. It is the first time that antioxidant capacity in plasma is evaluated in AD patients characterized by their APOE genotypes. © 2005 EFNS.
2015-09-14T09:57:30Z
2015-09-14T09:57:30Z
2005
2015-09-14T09:57:31Z
artículo
European Journal of Neurology 12: 531- 535 (2005)
http://hdl.handle.net/10261/122024
10.1111/j.1468-1331.2005.01000.x
eng
Sí
closedAccess
Wiley-Blackwell