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000137263 0247_ $$2doi$$a10.3233/JAD-131469
000137263 0247_ $$2pmid$$apmid:24217274
000137263 0247_ $$2ISSN$$a1387-2877
000137263 0247_ $$2ISSN$$a1875-8908
000137263 037__ $$aDZNE-2020-03585
000137263 041__ $$aEnglish
000137263 082__ $$a610
000137263 1001_ $$0P:(DE-HGF)0$$aTzikas, Stergios$$b0
000137263 245__ $$aIncreased myeloperoxidase plasma levels in patients with Alzheimer's disease.
000137263 260__ $$aAmsterdam$$bIOS Press$$c2014
000137263 264_1 $$2Crossref$$3print$$bIOS Press$$c2014-02-07
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000137263 520__ $$aIncreasing evidence supports the role of cardiovascular risk factors in the development of Alzheimer’s disease (AD).Objective:In the present pilot study, we investigated plasma concentrations of myeloperoxidase (MPO) and its possible association with plasma amyloid-β (Aβ)1-42/1-40 ratio in AD patients and elderly healthy controls.Methods:The study sample included 28 AD patients and 27 elderly individuals with a normal cognitive status as a control group. The Mini-Mental Status Examination was used to determine the global cognition. MPO, Aβ1-40, and Aβ1-42 plasma concentrations were measured by enzyme linked immunoabsorbent assays.Results:AD patients showed significantly higher plasma concentrations of MPO in comparison to healthy elderly controls (AD versus healthy elderly controls (mean ± SD): 132.8 ± 114.8 ng/mL versus 55.0 ± 42.6 ng/mL; p = 0.002). MPO plasma concentrations showed a significant positive correlation in the whole sample with the presence of AD (ρ = 0.428, p < 0.001) and its stage (ρ = 0.331; p = 0.013) as well as with plasma concentrations of Aβ1-42 (ρ = 0.406; p = 0.004) and Aβ1-42/1-40 ratio (ρ = 0.354; p = 0.013). In a binary logistic regression model, plasma MPO concentrations were independently associated with the presence of AD (p = 0.014).Conclusion:AD patients showed significantly increased plasma levels of MPO, which could be an important molecular link between atherosclerosis and AD. Further studies should evaluate whether MPO may also be a useful biomarker and potential new treatment target in AD.
000137263 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
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000137263 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000137263 650_7 $$2NLM Chemicals$$aPeptide Fragments
000137263 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-40)
000137263 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-42)
000137263 650_7 $$0EC 1.11.1.7$$2NLM Chemicals$$aPeroxidase
000137263 650_2 $$2MeSH$$aAged
000137263 650_2 $$2MeSH$$aAged, 80 and over
000137263 650_2 $$2MeSH$$aAlzheimer Disease: blood
000137263 650_2 $$2MeSH$$aAmyloid beta-Peptides: blood
000137263 650_2 $$2MeSH$$aFemale
000137263 650_2 $$2MeSH$$aHumans
000137263 650_2 $$2MeSH$$aImmunoenzyme Techniques
000137263 650_2 $$2MeSH$$aLogistic Models
000137263 650_2 $$2MeSH$$aMale
000137263 650_2 $$2MeSH$$aMental Status Schedule
000137263 650_2 $$2MeSH$$aNeuropsychological Tests
000137263 650_2 $$2MeSH$$aPeptide Fragments: blood
000137263 650_2 $$2MeSH$$aPeroxidase: blood
000137263 650_2 $$2MeSH$$aROC Curve
000137263 7001_ $$0P:(DE-HGF)0$$aSchlak, Dennis$$b1
000137263 7001_ $$0P:(DE-HGF)0$$aSopova, Kateryna$$b2
000137263 7001_ $$0P:(DE-HGF)0$$aGatsiou, Aikaterini$$b3
000137263 7001_ $$0P:(DE-HGF)0$$aStakos, Dimitrios$$b4
000137263 7001_ $$0P:(DE-HGF)0$$aStamatelopoulos, Kimon$$b5
000137263 7001_ $$0P:(DE-HGF)0$$aStellos, Konstantinos$$b6$$eCorresponding author
000137263 7001_ $$0P:(DE-2719)2000055$$aLaske, Christoph$$b7$$eLast author
000137263 77318 $$2Crossref$$3journal-article$$a10.3233/jad-131469$$b : IOS Press, 2014-02-07$$n3$$p557-564$$tJournal of Alzheimer's Disease$$v39$$x1875-8908$$y2014
000137263 773__ $$0PERI:(DE-600)2070772-1$$a10.3233/JAD-131469$$gVol. 39, no. 3, p. 557 - 564$$n3$$p557-564$$q39:3<557 - 564$$tJournal of Alzheimer's disease$$v39$$x1875-8908$$y2014
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