Outlining a Population “at Risk” of Parkinson’s Disease: Evidence from a Case-Control Study

Schirinzi, Tommaso; Martella, Giuseppina; D'Elia, Alessio; Lazzaro, Giulia Di; Imbriani, Paola; Madeo, Graziella; Monaco, Leonardo; Maltese, Marta; Pisani, Antonio

doi:10.1155/2016/9646057

Cited by 6 publications

(3 citation statements)

References 42 publications

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“…We performed a screening of the abstracts of all original articles, and publications in abstract form were excluded from further analysis. The initial selection included 76 studies measuring CSF, serum/plasma or urine levels of iron, ferritin, transferrin, lactoferrin, haptoglobin, and or hepcidine [6,9–83]. Table 2 summarizes the methods used for the determinations, the main results, and observations in some of these studies, including the reason for exclusion of several of these studies from the meta‐analysis.…”

Section: Methodsmentioning

confidence: 99%

Biological fluid levels of iron and iron‐related proteins in Parkinson’s disease: Review and meta‐analysis

Jiménez‐Jiménez

Alonso‐Navarro

García‐Martín

et al. 2020

Euro J of Neurology

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Background and purpose Several studies suggested a role or iron in the pathogenesis or Parkinson's disease (PD), and substantia nigra iron concentrarions have been found increased in PD. However, the results on cerebrospinal (CSF) and serum/plasma iron levels in PD patients have been controversial. The aim of this systematic review and meta‐analysis was to establish the CSF and serum/plasma levels of iron and iron‐related proteins (ferritin, transferrin, lactoferrin, haptoglobin, and hepcidine) levels, and the urine levels of iron, in patients with PD. Methods Four databases (PubMed, EMBASE, MedLine, and Web of Science – Core Collection) were reviewed for studies published from 1966 to October 5, 2020. References of interest were identified. A meta‐analysis of eligible studies was performed according to the Preferred Reporting Items for Systematic Reviews and Meta‐analyses (PRISMA) and Meta‐analysis of Observational Studies in Epidemiology (MOOSE) guidelines, using the R software package meta. Results A non‐significant trend towards higher CSF iron levels and marginally significantly lower serum/plasma iron levels was observed in patients with PD compared with age‐ and sex‐matched controls. CSF and serum/plasma ferritin and transferrin concentrations, and serum/plasma lactoferrin and haptoglobin concentrations did not differ significantly between PD patients and controls. Conclusion The findings of this study suggest an association between decreased serum/plasma iron levels and, possibly, higher CSF iron levels with risk of PD.

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Section: Methodsmentioning

confidence: 99%

Biological fluid levels of iron and iron‐related proteins in Parkinson’s disease: Review and meta‐analysis

Jiménez‐Jiménez

Alonso‐Navarro

García‐Martín

et al. 2020

Euro J of Neurology

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“…PD causes a progressive and disabling syndrome, including motor and non-motor disturbances, which severely impair patients' quality of life. Therefore, effective disease modifying treatments represent an unmet clinical need (1–3).…”

Section: Introductionmentioning

confidence: 99%

Dietary Vitamin E as a Protective Factor for Parkinson's Disease: Clinical and Experimental Evidence

et al. 2019

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Effective disease-modifying treatments are an urgent need for Parkinson's disease (PD). A putative successful strategy is to counteract oxidative stress, not only with synthetic compounds, but also with natural agents or dietary choices. Vitamin E, in particular, is a powerful antioxidant, commonly found in vegetables and other components of the diet. In this work, we performed a questionnaire based case-control study on 100 PD patients and 100 healthy controls. The analysis showed that a higher dietary intake of Vitamin E was inversely associated with PD occurrence independently from age and gender (OR = 1.022; 95% CI = 0.999–1.045; p < 0.05), though unrelated to clinical severity. Then, in order to provide a mechanistic explanation for such observation, we tested the effects of Vitamin E and other alimentary antioxidants in vitro , by utilizing the homozygous PTEN-induced kinase 1 knockout ( PINK1 −/− ) mouse model of PD. PINK1 −/− mice exhibit peculiar alterations of synaptic plasticity at corticostriatal synapses, consisting in the loss of both long-term potentiation (LTP) and long-term depression (LTD), in the absence of overt neurodegeneration. Chronic administration of Vitamin E (alpha-tocopherol and the water-soluble analog trolox) fully restored corticostriatal synaptic plasticity in PINK1 −/− mice, suggestive of a specific protective action. Vitamin E might indeed compensate PINK1 haploinsufficiency and mitochondrial impairment, reverting some central steps of the pathogenic process. Altogether, both clinical and experimental findings suggest that Vitamin E could be a potential, useful agent for PD patients. These data, although preliminary, may encourage future confirmatory trials.

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“…Refs. [ 271 , 272 , 273 , 274 , 275 , 276 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 , 288 , 289 , 290 ] are cited in the Supplementary Materials file .…”

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confidence: 99%

Abnormalities in Copper Status Associated with an Elevated Risk of Parkinson’s Phenotype Development

Karpenko,

Muruzheva,

Ilyechova

et al. 2023

Antioxidants

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In the last 15 years, among the many reasons given for the development of idiopathic forms of Parkinson’s disease (PD), copper imbalance has been identified as a factor, and PD is often referred to as a copper-mediated disorder. More than 640 papers have been devoted to the relationship between PD and copper status in the blood, which include the following markers: total copper concentration, enzymatic ceruloplasmin (Cp) concentration, Cp protein level, and non-ceruloplasmin copper level. Most studies measure only one of these markers. Therefore, the existence of a correlation between copper status and the development of PD is still debated. Based on data from the published literature, meta-analysis, and our own research, it is clear that there is a connection between the development of PD symptoms and the number of copper atoms, which are weakly associated with the ceruloplasmin molecule. In this work, the link between the risk of developing PD and various inborn errors related to copper metabolism, leading to decreased levels of oxidase ceruloplasmin in the circulation and cerebrospinal fluid, is discussed.

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Outlining a Population “at Risk” of Parkinson’s Disease: Evidence from a Case-Control Study

Cited by 6 publications

References 42 publications

Biological fluid levels of iron and iron‐related proteins in Parkinson’s disease: Review and meta‐analysis

Biological fluid levels of iron and iron‐related proteins in Parkinson’s disease: Review and meta‐analysis

Dietary Vitamin E as a Protective Factor for Parkinson's Disease: Clinical and Experimental Evidence

Abnormalities in Copper Status Associated with an Elevated Risk of Parkinson’s Phenotype Development

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