Ceruloplasmin and superoxide dismutase (SOD1) in Parkinson's disease: A follow-up study

Tórsdóttir, Gudlaug; Sveinbjörnsdóttir, Sigurlaug; Kristinsson, Jakob; Snædal, Jón; Jóhannesson, Torkell

doi:10.1016/j.jns.2005.10.015

Cited by 36 publications

(31 citation statements)

References 25 publications

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“…1 c). Our findings are in concordance with previous studies showing lower serum ceruloplasmin in PD [9,11]. We did not, however, find a correlation between serum ceruloplasmin and duration of PD, or with the current age.…”

Section: Discussionsupporting

confidence: 92%

“…In contrast, a previous study by Tórsdót-tir et al [9] showed a decrease in ceruloplasmin with duration of PD. However, the authors were unable to replicate this finding in their follow-up study [11]. Also, in their later study, ceruloplasmin levels did not differ between early (Hoehn & Yahr II and III), and later stage (IV & V) PD [11], once again suggesting that neither duration nor severity of PD could explain lower ceruloplasmin levels.…”

Section: Discussionmentioning

confidence: 82%

“…In contrast, Loeffler et al demonstrated that brain ceruloplasmin immunoreactivity is increased in PD and attributed this finding to an acute phase response to oxidative stress [10]. Subsequently, a more recent study of serum ceruloplasmin in PD by Tórsdóttir et al [11] confirmed their earlier findings of lower levels in PD as opposed to controls. Another study of ceruloplasmin in spinal fluid in treated and untreated PD found reduced levels compared to controls [12], suggesting that serum ceruloplasmin may provide an indirect measure of brain levels.…”

Section: Introductionmentioning

confidence: 94%

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Lower serum ceruloplasmin levels correlate with younger age of onset in Parkinson’s disease

Bharucha

Vincent³

et al. 2008

J Neurol

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Ceruloplasmin functions as a ferroxidase in iron metabolism. Parkinson's disease (PD) is characterized by an increase in brain iron. We postulated that lower circulating ceruloplasmin levels in PD would result in rapid brain iron accumulation and an earlier age of onset. Consecutive PD patients were separated into subgroups with younger (< or = 60 years, n = 62) and older ages of onset (> 60, n = 29), and compared to non-PD controls (n = 40). A one-way ANOVA comparing ceruloplasmin levels showed a very robust effect [F(2,128) = 46.4, p < 1e-99]. Post hoc analysis demonstrated that the younger-onset PD subgroup [22.0 mg/dl +/- 6.5 SD] had a lower mean ceruloplasmin level compared to the older-onset PD subgroup [35.7 +/- 10.4] and controls [35.6 +/- 8.4], whose levels did not differ from each other. Ceruloplasmin levels showed robust correlation with age of onset in all 91 PD patients [r = 0.56, r(2) = 0.31, p < 0.0001] but not in the non-PD controls [r = 0.16, r(2) = 0.03, not significant]. Mode of onset and duration of PD showed no relationship to ceruloplasmin. Serum copper and ferritin, available in most patients, did not differ between the PD subgroups. Younger-onset PD patients have significantly lower levels of serum ceruloplasmin compared to those with older-onset PD. Ceruloplasmin may play a role in the etiopathogenesis of younger-onset PD patients and merits further study.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 94%

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Lower serum ceruloplasmin levels correlate with younger age of onset in Parkinson’s disease

Bharucha

Vincent³

et al. 2008

J Neurol

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“…A retrospective study by Walshe reported that the serum Cp levels were less than the lower limit of normal range in almost half of all patients with non-Wilsonian movement disorders [12]. The serum levels and oxidative activity of Cp in 40 PD patients were noted to be lower than in their age- and gender-matched controls [13]. While the authors proposed that old age, long disease duration and long term use of L -dopa might have contributed to the reduction in Cp levels in these PD patients, these factors were not shown to influence the Cp levels among our PD patients.…”

Section: Discussionmentioning

confidence: 99%

Reduced Serum Caeruloplasmin Levels in Non-Wilsonian Movement Disorders

Ling

Bhidayasiri²

2011

Eur Neurol

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Reduction in caeruloplasmin (Cp) levels is sometimes found in other sporadic movement disorders, not limited to Wilson’s disease (WD). Serum levels of Cp, copper, iron and gamma-glutamyl transpeptidase were measured in 71 patients with various diagnoses of movement disorders, including Parkinson’s disease (PD), atypical parkinsonian disorders, tardive dyskinesia, essential tremor, and idiopathic focal dystonia, and compared with those of 26 healthy age- and gender-matched controls. The mean Cp level in the patient group was 20.5 ± 4.2 mg/dl , lower than in controls (23.5 ± 7.2 mg/dl; p = 0.005). In subgroup analysis, mean Cp level of PD patients (19.6 ± 3.0 mg/dl) was lower than that of controls (p = 0.045). In a group analysis as neurodegenerative movement disorders (NDD), their mean Cp level was 19.9 ± 3.0 mg/dl, lower than that of controls (p = 0.019). Linear regression analysis indicated that the presence of NDD was the main factor associated with lower Cp levels. The finding of reduced serum Cp level in non-Wilsonian movement disorders and selective reduction in the neurodegenerative subgroup supports the notion that Cp might be associated with the cascade of neurotoxicity in NDD. The variation in Cp level in other non-WD conditions highlights the fact that Cp level is a poor screening test for WD in the absence of clear clinical suspicion.

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“…Three forms of SOD exist in humans and other mammals: SOD1 is located in the cytoplasm, SOD2 in the mitochondria, while SOD3 is extracellular. Mutations in SOD lead to diseases commonly associated with high oxidative stress such as familial amyotrophic lateral sclerosis, Parkinson's Disease, and cardiovascular disease (Fukai et al, 2002;Noor et al, 2002;Tórsdóttir et al, 2006). Overexpression of SOD inhibits LDL oxidation by endothelial cells (Fang et al, 1998).…”

Section: Rosmentioning

confidence: 99%