Journals / Türk Nöroloji Dergisi / 2016 / Cilt: 22 - Sayı: 1

The Role of Ceruloplasmin in Neurodegeneration in Parkinson's Disease

İdiyopatik Parkinson Hastalığında Serüloplazminin Nörodejenerasyonda Rolü

Pages
19–25
Publication Date
2022-11-05
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)

Also in the IPD group, CL NAA/Cho and NAA/Cr ratios were significantly lower than the ipsilateral (IL) values (p

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Oxidative stress has been implicated to play a major role in the neuronal cell death in idiopathic Parkinson's disease (IPD).
📊
Key Findings & Data:The aim of this study was to determine the serum ceruloplasmin levels in patients with IPD and evaluate its role in neurodegeneration using hydrogen proton magnetic resonance spectroscopic imaging (H-1 MRSI).Materials and Methods: Twenty-three patients with the IPD and 12 healthy controls were studied using single-voxel H-1 MRSI of the bilateral putamen.
💡
Conclusion & Impact:Also in the IPD group, CL NAA/Cho and NAA/Cr ratios were significantly lower than the ipsilateral (IL) values (p
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Oxidative stress has been implicated to play a major role in the neuronal cell death in idiopathic Parkinson's disease (IPD). Ceruloplasmin is a ferroxidase that oxidizes toxic ferrous iron to its nontoxic ferric form and thus helps prevent oxidative damage to proteins, lipids, and DNA. The aim of this study was to determine the serum ceruloplasmin levels in patients with IPD and evaluate its role in neurodegeneration using hydrogen proton magnetic resonance spectroscopic imaging (H-1 MRSI).Materials and Methods: Twenty-three patients with the IPD and 12 healthy controls were studied using single-voxel H-1 MRSI of the bilateral putamen. The peak ratios of N-acetyl aspartate (NAA) to creatinine (Cr) and choline (Cho) were measured in both groups and serum ceruloplasmin levels were detected. Results: Compared with the controls, the ratios of NAA/Cho and NAA/Cr in putamen contralateral (CL) to the symptomatic limbs were significantly lower in patients with IPD. Also in the IPD group, CL NAA/Cho and NAA/Cr ratios were significantly lower than the ipsilateral (IL) values (p

Özet

Amaç: İdiyopatik Parkinson hastalığında (İPH) oksidatif stres nöronal hücre ölümü üzerinde majör role sahiptir. Serüloplazmin ferrooksidaz aktivitesi ile ferröz demiri ferrik forma okside eder ve böylece hücrenin DNA, lipid ve protein bileşenlerini oksidatif hasardan korur. Bizim çalışmamızda proton manyetik rezonans spektroskopi (H-1 MRS) ile serüloplazmin eksikliğinin nörodejenerasyon üzerindeki etkisi araştırılmıştır.Gereç ve Yöntem: İPH tanılı 23 hasta ve 12 sağlıklı kontrol olguda iki yanlı putamen tek voksel H-1 MRS yöntemiyle incelendi. Her iki grupta N-asetil aspartat (NAA), kreatin (Cr) ve kolin (Cho) pik değerleri ve serum serüloplazmin düzeyleri belirlendi. Bulgular: İPH hastalarında semptomatik ekstremitenin kontralateral (KL) putaminal bölge NAA/Cho ve NAA/Cr oranı kontrol grubuna kıyasla anlamlı derecede düşüktü. Ayrıca İPH grubunda KL NAA/Cho ve NAA/Cr oranları ipsilateraline (İL) göre anlamlı derecede düşüktü (p

🔖

Cite This Article

AYAZ, T., GÖKÇE, D., IŞIK, N., AYDIN, Ş., GÜRER, R. (2022). The Role of Ceruloplasmin in Neurodegeneration in Parkinson's Disease. Türk Nöroloji Dergisi, Cilt: 22 - Sayı: 1, 19–25. https://ajindex.com/articles/636933

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Dawson TM, Dawson VL. Molecular pathways of neurodegeneration in Parkinson's disease. Science 2003;302:819-822
  2. Litvan I, Chesselet MF, Gasser T, Di Monte DA, Parker D Jr, Hagg T, Hardy J, Jenner P, Myers RH, Price D, Hallett M, Langston WJ, Lang AE, Halliday G, Rocca W, Duyckaerts C, Dickson DW, Ben-Shlomo Y, Goetz CG, Melamed E. The etiopathogenesis of Parkinson disease and suggestions for future research. Part II J Neuropathol Exp Neurol 2007;66:329-336
  3. Beal MF. Aging, energy and oxidative stress in neurodegenerative diseases. Ann Neurol 1995;38:357-366
  4. Halliwell B. Oxygen radicals as key mediators in neurological disease: Fact or fiction? Ann Neurol 1992;32:10-15
  5. Jenner P. Oxidative damage in neurodegenerative disease. Lancet 1994;344:796-798
  6. Damier P, Hirsch EC, Agid Y, Graybiel AM. The substantia nigra of the human brain II. Patterns of loss of dopamine-containing neurons in Parkinson's disease. Brain 1999;122:1437-1448
  7. Braak H, Del Tredici K, Rüb U, de Vos RA, Jansen Steur EN, Braak E. Staging of brain pathology related to sporadic Parkinson's disease. Neurobiol Aging 2003;24:197-211
  8. Graham JM, Paley MN, Grünewald RA, Hoggard N, Griffiths PD. Brain iron deposition in Parkinson's disease imaged using the PRIME magnetic resonance sequence. Brain 2000;123:2423-2431
  9. Zecca L, Youdim MB, Riederer P, Connor JR, Crichton RR. Iron, brain ageing and neurodegenerative disorders. Nat Rev Neurosci 2004;5:863-873
  10. Altamura S, Muckenthaler MU. Iron toxicity in diseases of aging: Alzheimer's disease, Parkinson's disease and atherosclerosis. JAlzheimer's Dis 2009;16:879-895
  11. Barnham KJ, Masters CL, Torsdottir G, Bush AI. Neurodegenerative diseases and oxidative stress. Nat Rev Drug Discov 2004;3:205-214
  12. Dexter DT, Carayon A, Javoy-Agid F, Agid Y, Wells FR, Daniel SE, Lees AJ, Jenner P, Marsden CD. Alterations in the levels of iron, ferritin and other trace metals in Parkinson's disease and other neurodegenerative diseases affecting the basal ganglia. Brain 1991;114:1953-1975
  13. Berg D, Hochstrasser H. Iron metabolism in Parkinsonian syndromes. Mov Disord 2006;21:1299-1310
  14. Rhodes SL, Ritz B. Genetics of iron regulation and the possible role of iron in Parkinson's disease. Neurobiol Dis 2008;32:183-195
  15. Loeffler DA, Connor JR, Juneau PL, Snyder BS, Kanaley L, DeMaggio AJ, Nguyen H, Brickman CM, Lewitt PA. Transferrin and iron in normal, Alzheimer's disease, and Parkinson's disease brain regions. J Neurochem 199