001     137263
005     20240321220223.0
024 7 _ |a 10.3233/JAD-131469
|2 doi
024 7 _ |a pmid:24217274
|2 pmid
024 7 _ |a 1387-2877
|2 ISSN
024 7 _ |a 1875-8908
|2 ISSN
037 _ _ |a DZNE-2020-03585
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Tzikas, Stergios
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Increased myeloperoxidase plasma levels in patients with Alzheimer's disease.
260 _ _ |a Amsterdam
|c 2014
|b IOS Press
264 _ 1 |3 print
|2 Crossref
|b IOS Press
|c 2014-02-07
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
|b journal
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|0 PUB:(DE-HGF)16
|s 1710945505_2066
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Increasing 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.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Peptide Fragments
|2 NLM Chemicals
650 _ 7 |a amyloid beta-protein (1-40)
|2 NLM Chemicals
650 _ 7 |a amyloid beta-protein (1-42)
|2 NLM Chemicals
650 _ 7 |a Peroxidase
|0 EC 1.11.1.7
|2 NLM Chemicals
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Aged, 80 and over
|2 MeSH
650 _ 2 |a Alzheimer Disease: blood
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: blood
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Immunoenzyme Techniques
|2 MeSH
650 _ 2 |a Logistic Models
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mental Status Schedule
|2 MeSH
650 _ 2 |a Neuropsychological Tests
|2 MeSH
650 _ 2 |a Peptide Fragments: blood
|2 MeSH
650 _ 2 |a Peroxidase: blood
|2 MeSH
650 _ 2 |a ROC Curve
|2 MeSH
700 1 _ |a Schlak, Dennis
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Sopova, Kateryna
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Gatsiou, Aikaterini
|0 P:(DE-HGF)0
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700 1 _ |a Stakos, Dimitrios
|0 P:(DE-HGF)0
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700 1 _ |a Stamatelopoulos, Kimon
|0 P:(DE-HGF)0
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700 1 _ |a Stellos, Konstantinos
|0 P:(DE-HGF)0
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|e Corresponding author
700 1 _ |a Laske, Christoph
|0 P:(DE-2719)2000055
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|e Last author
773 1 8 |a 10.3233/jad-131469
|b : IOS Press, 2014-02-07
|n 3
|p 557-564
|3 journal-article
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|t Journal of Alzheimer's Disease
|v 39
|y 2014
|x 1875-8908
773 _ _ |a 10.3233/JAD-131469
|g Vol. 39, no. 3, p. 557 - 564
|0 PERI:(DE-600)2070772-1
|n 3
|q 39:3<557 - 564
|p 557-564
|t Journal of Alzheimer's disease
|v 39
|y 2014
|x 1875-8908
856 4 _ |u https://pub.dzne.de/record/137263/files/DZNE-2020-03585_Restricted.pdf
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