Ceruloplasmin in Parkinson's disease and the nonmotor symptoms

Abstract

ObjectivesTo investigate the relationship between ceruloplasmin (CP) and Parkinson's disease (PD), and the correlation between CP level and the time difference between nonmotor symptoms and motor symptoms and the diagnosis were also mentioned.Materials and MethodsSixty‐six patients diagnosed with PD for the first time were included in the study. They were divided into CP reduction group (31 cases) and CP normal group (35 cases) according to their CP level. The estimated time difference between nonmotor symptoms and motor symptoms and the diagnosis were recorded respectively. The magnetic sensitive nigra phase value was measured by susceptibility weighted imaging (SWI).ResultsCeruloplasmin level was middling correlated with age (r = .561, p < .001). There was strong negative correlation between CP level and UPDRS scores (r = −.727, p < .001). The CP level was significantly correlated with the magnetic sensitive nigra phase value (r = .891, p < .001). CP level showed moderate correlation with the time difference from nonmotor symptoms to motor symptoms (r = .559, p < .001), besides, the time difference between nonmotor symptoms and the diagnosis (r = .525, p < .001) and CP level was also moderately related.ConclusionsCeruloplasmin interference in iron metabolism was closely related with PD development. And there were slight corrections between CP level and the time difference from nonmotor symptoms to motor symptoms or the diagnosis.

The Role of Genetic Testing in the Clinical Practice and Research of Early-Onset Parkinsonian Disorders in a Hungarian Cohort: Increasing Challenge in Genetic Counselling, Improving Chances in Stratification for Clinical Trials

“…Moreover, other authors suggested that heterozygous mutations in PLA2G6 may also contribute to the susceptibility for developing PD (Ferese et al, 2018), as some PLA2G6 heterozygous mutations were presented in PD patients (Bower et al, 2011; Lu et al, 2012). We assume that the I898M damaging mutation in the CP gene, which plays an important role in the iron and copper metabolism in the brain (Zhao et al, 2018), could intensify the risk of developing PD. These four patients in Table 5 with a mean AOO (42 ± 5.72 years) is rather like the sporadic patients with a single genetic risk variant presented in Table 3 with a mean AAO (40 ± 6.94 years) than the sporadic patients with potential oligogenic background (presented in Table 4 with a mean AOO 34.5 ± 4.95 years).…”

Ferroptosis and its potential role in the physiopathology of Parkinson’s Disease

“…In addition, APP expression is decreased in the SN of PD patients, leading to a similar iron-associated phenotype as APP knockout mice 66,68 . Furthermore, the ferroxidase activity of CP required to facilitate iron efflux through FPN is decreased in both patients and animal models of PD 108,109 . Further support for iron elevation as a cause of parkinsonian pathology comes from the genetic disorder aceruloplasminemia, in which CP is mutated, often leading to a parkinsonian phenotype including gait difficulties, ataxia, involuntary movements and cognitive decline that correlate with brain iron deposition 110,111 .…”

Exploring the Genetic and Genomic Connection Underlying Neurodegeneration with Brain Iron Accumulation and the Risk for Parkinson’s Disease

“…There have been reports linking lower CP levels with PD development, and CP gene mutations have been associated with substantia nigra hyperechogenicity using transcranial sonography. 38 Additionally, hyperechogenicity is a common finding in idiopathic PD patients and many studies suggest that it is an important risk marker of future PD . 39,40 One mutation associated with SN hyperechogenicity is p.R793H.…”