Relationship of cognitive performance with prolidase and oxidative stress in Alzheimer disease

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dc.contributor.authorArikanoglu, Adalet
dc.contributor.authorAkil, Esref
dc.contributor.authorVarol, Sefer
dc.contributor.authorYucel, Yavuz
dc.contributor.authorYuksel, Hatice
dc.contributor.authorCevik, Mehmet Ugur
dc.contributor.authorPalanci, Yilmaz
dc.date.accessioned2024-04-24T16:02:00Z
dc.date.available2024-04-24T16:02:00Z
dc.date.issued2013
dc.departmentDicle Üniversitesien_US
dc.description.abstractGlutamate excitotoxicity and oxidative stress are held responsible for the pathogenesis of Alzheimer's disease (AD). Prolidase is known to have a crucial part in the recycling of proline for collagen synthesis. Elevated proline levels have been shown to increase glutamate concentration. To our knowledge, prolidase activity in AD has not yet been studied. In this study, we aimed to reveal the relationship of AD with oxidative stress and collagen turnover by comparing AD patients and healthy control group with regard to total antioxidant status (TAS), total oxidant status (TOS), and prolidase levels. Fifty patients (mean age, 72.5 +/- A 8.9 years) diagnosed with AD and a control group comprised of 39 healthy individuals (mean age, 69.1 +/- A 7.1 years) were compared relative to serum TAS, TOS, and prolidase levels. The relationship of cognitive performance with prolidase, TAS, and TOS was evaluated by Mini mental state examination (MMSE). Alzheimer's disease group demonstrated statistically significantly higher prolidase and TOS levels as compared to the control group (p = 0.01, p = 0.018, respectively). Total antioxidant status level was significantly lower in the dementia group than in the control group (p = 0.032). MMSE manifested a negative correlation with prolidase and TOS levels (p = 0.001, r = -0.33; p = 0.002, r = -0.32, respectively), while displaying a positive correlation with TAS levels (p = 0.002, r = 0.32). In conclusion, elevated prolidase and TOS levels along with reduced TAS concentrations suggest that oxidative stress and collagen breakdown are involved in the cognitive impairment in AD.en_US
dc.identifier.doi10.1007/s10072-013-1346-4
dc.identifier.endpage2121en_US
dc.identifier.issn1590-1874
dc.identifier.issn1590-3478
dc.identifier.issue12en_US
dc.identifier.pmid23479033
dc.identifier.scopus2-s2.0-84890571330
dc.identifier.scopusqualityQ1
dc.identifier.startpage2117en_US
dc.identifier.urihttps://doi.org/10.1007/s10072-013-1346-4
dc.identifier.urihttps://hdl.handle.net/11468/14567
dc.identifier.volume34en_US
dc.identifier.wosWOS:000328209500005
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherSpringer-Verlag Italia Srlen_US
dc.relation.ispartofNeurological Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAlzheimer's Diseaseen_US
dc.subjectProlidaseen_US
dc.subjectOxidative Stressen_US
dc.subjectCognitive Performanceen_US
dc.titleRelationship of cognitive performance with prolidase and oxidative stress in Alzheimer diseaseen_US
dc.titleRelationship of cognitive performance with prolidase and oxidative stress in Alzheimer disease
dc.typeArticleen_US

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