The Role of Ceruloplasmin in Neurodegeneration in Parkinson’s Disease

• Main Authors: Reyhan Gürer, Şenay Aydın, Dilvin Gökçe
• Format: Article
• Language: English
• Published: Galenos Yayinevi 2016-04-01
• Series: Türk Nöroloji Dergisi
• Subjects: Idiopathic Parkinson’s disease; proton magnetic resonance spectroscopy; ceruloplasmin
• Online Access: http://www.tjn.org.tr/jvi.aspx?pdir=tjn&plng=eng&un=TJN-58751&look4=

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<0.001). There was no significant difference between ratios of metabolites in putamen IL to the symptomatic limbs in the IPD group compared with the healthy controls. The mean serum ceruloplasmin level of IPD patients was significantly lower than that of the control group (p<0.001). In the IPD group, a significant direct correlation was found between levels of ceruloplasmin and CL putamen NAA/Cho ratio (p=0.011). Conclusion: In our study the direct correlation between low levels of ceruloplasmin and CL putamen NAA/Cho ratio supports the hypothesis that ceruloplasmin deficiency may contribute to free radical-induced death of neuronal cells.