Journals / Turkish Journal of Medical Sciences / 2015 / Cilt: 45 - Sayı: 5

Plasma 8-isoPGF2? and serum melatonin levels in patients with minimal cognitive impairment and Alzheimer disease

Pages
1073–1077
Publication Date
2015-12-04
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Although the plasma 8-isoPGF2α and serum melatonin levels in MCI were not found to be good early diagnostic markers to indicate risk of AD, results were found to support the role of oxidative stress in AD.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/aim: F2α-isoprostane is accepted as an oxidative stress indicator and melatonin shows neuroprotective effects by antioxidative and antiamyloidogenic influences.
📊
Key Findings & Data:By measuring these in patients diagnosed with minimal cognitive impairment (MCI) and Alzheimer-type dementia, we intended to demonstrate whether the measurement of these markers contributes to early diagnosis of Alzheimer disease (AD) in the MCI stage or not.
💡
Conclusion & Impact:Conclusion: Although the plasma 8-isoPGF2α and serum melatonin levels in MCI were not found to be good early diagnostic markers to indicate risk of AD, results were found to support the role of oxidative stress in AD.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Alzheimer disease · minimal cognitive impairment · oxidative stress

Abstract

Background/aim: F2&alpha;-isoprostane is accepted as an oxidative stress indicator and melatonin shows neuroprotective effects by antioxidative and antiamyloidogenic influences. By measuring these in patients diagnosed with minimal cognitive impairment (MCI) and Alzheimer-type dementia, we intended to demonstrate whether the measurement of these markers contributes to early diagnosis of Alzheimer disease (AD) in the MCI stage or not. Materials and methods: Three groups (n = 63) were created: the AD group, MCI group, and control group. Serum melatonin levels were measured by radioimmunoassay method, and plasma total 8-isoPGF2&alpha; levels were measured by enzyme immunoassay method. Results: Significant differences were observed in the melatonin levels between the MCI group and AD group (P = 0.009), and in 8-isoPGF2&alpha; levels between the AD group and control group (P = 0.022). A negative correlation between mini-mental state examination (MMSE) scores and 8-isoPGF2&alpha; levels (r = -0.459, P < 0.001) and positive correlation between MMSE scores and melatonin levels (r = 0.317, P = 0.011) were found. Conclusion: Although the plasma 8-isoPGF2&alpha; and serum melatonin levels in MCI were not found to be good early diagnostic markers to indicate risk of AD, results were found to support the role of oxidative stress in AD.

Özet

Background/aim: F2&alpha;-isoprostane is accepted as an oxidative stress indicator and melatonin shows neuroprotective effects by antioxidative and antiamyloidogenic influences. By measuring these in patients diagnosed with minimal cognitive impairment (MCI) and Alzheimer-type dementia, we intended to demonstrate whether the measurement of these markers contributes to early diagnosis of Alzheimer disease (AD) in the MCI stage or not. Materials and methods: Three groups (n = 63) were created: the AD group, MCI group, and control group. Serum melatonin levels were measured by radioimmunoassay method, and plasma total 8-isoPGF2&alpha; levels were measured by enzyme immunoassay method. Results: Significant differences were observed in the melatonin levels between the MCI group and AD group (P = 0.009), and in 8-isoPGF2&alpha; levels between the AD group and control group (P = 0.022). A negative correlation between mini-mental state examination (MMSE) scores and 8-isoPGF2&alpha; levels (r = -0.459, P < 0.001) and positive correlation between MMSE scores and melatonin levels (r = 0.317, P = 0.011) were found. Conclusion: Although the plasma 8-isoPGF2&alpha; and serum melatonin levels in MCI were not found to be good early diagnostic markers to indicate risk of AD, results were found to support the role of oxidative stress in AD.

🔖

Cite This Article

ŞİRİN, F. B., DOĞUÇ, D. K., VURAL, H., EREN, İ., İNANLI, İ., SÜTCÜ, R., DELİBAŞ, N. (2015). Plasma 8-isoPGF2? and serum melatonin levels in patients with minimal cognitive impairment and Alzheimer disease. Turkish Journal of Medical Sciences, Cilt: 45 - Sayı: 5, 1073–1077. https://ajindex.com/articles/198436

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (10)

  1. Selekler K. Alzheimer hastalığının öncesi: hafif kognitif bozukluk. Hacettepe Tıp Dergisi 2004; 35: 199–206 (in Turkish). Petersen RC. Mild cognitive impairment: where are we? Alzheimer Dis Assoc Disord 2005; 19: 166–169. Chertkow H. Mild cognitive impairment. Curr Opin Neurol 2002; 15: 401–407. 4. Cardinalli DP, Vigo DE, Olivar N, Vidal MF, Furio AM, Brusco LI. Therapeutic application of melatonin in mild cognitive impairment. Am J Neurodegener Dis 2012; 1: 280–291.
  2. Braak H, Braak E. Diagnostic criteria for neuropathologic assessment of Alzheimer’s disease. Neurobiol Aging 1997; 18: 85–88.
  3. Montine TJ, Neely MD, Quinn JF, Beal F, Markesbery WR. Lipid peroxidation in aging brain and Alzheimer’s Disease. Free Radic Biol Med 2002; 33: 620–626. 7. Pratico D, Delanty N. Oxidative injury in diseases of the central nervous system: focus on Alzheimer’s disease. Am J Med 2000; 109: 577–585.
  4. Smith MA, Rottkamp C, Nunomura A, Raina AK, Perry G. Oxidative stress in Alzheimer’s disease. Biochim Biophys Acta 2000; 1502: 139–144. ChristenY. Oxidative stress and Alzheimer disease. Am J Clin Nutr 2000; 71: 621–629.
  5. Mariani E, Polidori MC, Cherubini A, Mecocci P. Oxidative stress in aging, neurodegenerative and vascular diseases: an overview. J Chromatogr B Analyt Technol Biomed Life Sci 2005; 827: 65–75. Praticò D, Lawson JA, Rokach J, FitzGerald GA. The isoprostanes in biology and medicine. Trends Endocrinol Metab 2001; 12: 243–247.
  6. Pratico D, Lawson JA, FitzGerald GA. Cyclooxygenase- dependent formation of the isoprostane, 8-epi PGF2α. J Biol Chem 1995; 270: 9800–9808. Reiter RJ. Melatonin: clinical relevance. Best Pract Res Clin Endocrinol Metab 2003; 17: 273–285.
  7. Matuszak Z, Reszka KJ, Chignell CF. Reaction of melatonin and related indoles with hydroxyl radicals: ESR and spin trapping investigations. Free Radic Biol Med 1997; 23: 367–372.
  8. Pappolla MA, Chyan YJ, Poeggeler B. An assessment of the antioxidant and antiamyloidogenic properties of melatonin: implications for Alzheimer’s disease. J Neural Transm 2000; 107: 203–231.
  9. Bettahi I, Pozo D, Osuna C, Reiter RJ, Acuna-Castroviejo D, Guerrero JM. Melatonin reduces nitric oxide synthase activity in rat hypothalamus. J Pineal Res 1996; 20: 205–210.
  10. Liu RY, Zhou JN, van Heerikhuize J, Hofman MA, Swaab DF. Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer’s disease, and apolipoprotein E-epsilon4/4 genotype. J Clin Endocrinol Metab 1999; 84: 323– 327. Wu YH, Swaab DF. The human pin