Serum levels of hepcidin and interleukin 6 in Parkinson’s disease

Kwiatek-Majkusiak, Jolanta; Geremek, Maciej; Koziorowski, Dariusz; Tomasiuk, Ryszard; Szlufik, Stanisław; Friedman, Andrzej

doi:10.21307/ane-2020-026

Cited by 21 publications

(19 citation statements)

References 35 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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“…The effect of other cytokines, acute phase response type 1 (including IL-1α, IL-1β, TNF-α and TNF-β), is indirect and requires more time after the activation of the inflammatory stimulus induces the secretion of IL-6, and it is only IL-6 that induces an increase in the production of hepcidin [ 192 ]. Kwiatek-Majkusiak et al showed that the serum concentrations of hepcidin and IL-6 in the group of all PD patients were significantly higher than in the control group [ 193 ]. Additionally, positive correlations between serum hepcidin and IL-6 were found in the PD group [ 193 ].…”

Section: Various Neurodegenerative Factorsmentioning

confidence: 99%

“…Kwiatek-Majkusiak et al showed that the serum concentrations of hepcidin and IL-6 in the group of all PD patients were significantly higher than in the control group [ 193 ]. Additionally, positive correlations between serum hepcidin and IL-6 were found in the PD group [ 193 ].…”

Section: Various Neurodegenerative Factorsmentioning

confidence: 99%

Mechanisms of Neurodegeneration in Various Forms of Parkinsonism—Similarities and Differences

Koziorowski

Figura

Milanowski

et al. 2021

Cells

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Parkinson's disease (PD), dementia with Lewy body (DLB), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA) belong to a group of neurodegenerative diseases called parkinsonian syndromes. They share several clinical, neuropathological and genetic features. Neurodegenerative diseases are characterized by the progressive dysfunction of specific populations of neurons, determining clinical presentation. Neuronal loss is associated with extra- and intracellular accumulation of misfolded proteins. The parkinsonian diseases affect distinct areas of the brain. PD and MSA belong to a group of synucleinopathies that are characterized by the presence of fibrillary aggregates of α-synuclein protein in the cytoplasm of selected populations of neurons and glial cells. PSP is a tauopathy associated with the pathological aggregation of the microtubule associated tau protein. Although PD is common in the world's aging population and has been extensively studied, the exact mechanisms of the neurodegeneration are still not fully understood. Growing evidence indicates that parkinsonian disorders to some extent share a genetic background, with two key components identified so far: the microtubule associated tau protein gene (MAPT) and the α-synuclein gene (SNCA). The main pathways of parkinsonian neurodegeneration described in the literature are the protein and mitochondrial pathways. The factors that lead to neurodegeneration are primarily environmental toxins, inflammatory factors, oxidative stress and traumatic brain injury.

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“…Activation of systemic inflammatory responses via an acute increase in proinflammatory cytokines, including interleukin-6 (IL-6) termed as Cytokine Storm, has been linked to disease severity and death in COVID-19 patients (Hashizume, 2020;Hojyo et al, 2020;Lukan, 2020). IL-6 like pro-inflammatory interleukins are also elevated in some neurodegenerative diseases such as Parkinson's disease (PD) (Kwiatek-Majkusiak et al, 2020), suggesting that patients with neurodegenerative diseases may be more susceptible to the severity of COVID-19. Although the relationship between COVID-19 severity and the progression of neurodegeneration diseases is not yet established, studies have shown that the COVID-19-related mortality rate is significantly higher in PD patients (Fasano et al, 2020;Zhang et al, 2020).…”

Section: Neurological Manifestations In Coronavirus Disease 2019mentioning

confidence: 99%

“…Edema and neuronal degeneration and the presence of SARS CoV particles or the viral genomic sequences together with circulating immune cells in different brain parts were identified in SARS-CoV infected patients ( Gu et al, 2005 ). Several studies related the SARS CoV infection in patients with late-stage SARS with neuronal and psychologic abnormalities ( Chan et al, 2006 ; Yip et al, 2010 ). Similar neurological observations, including encephalitis, infectious and toxic neuropathies, and Guillain-Barré syndrome, were found in coronavirus MERS-CoV infected patients ( Kim et al, 2017 ).…”

Section: Neurological Manifestations In Coronavirus Disease 2019mentioning

confidence: 99%

Neuronal and Cerebrovascular Complications in Coronavirus Disease 2019

Andrabi

2020

Front. Pharmacol.

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Coronavirus disease 2019 (COVID-19) is a pandemic disease resulting from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, primarily in the respiratory tract. This pandemic disease has affected the entire world, and the pathobiology of this disease is not yet completely known. The Interactions of SARS-CoV-2 proteins with different cellular components in the host cell may be necessary for understanding the disease mechanism and identifying crucial pharmacological targets in COVID-19. Studies have suggested that the effect of SARS-CoV-2 on other organs, including the brain, maybe critical for understanding the pathobiology of COVID-19. Symptoms in COVID-19 patients, including impaired consciousness dizziness, headache, loss of taste and smell, vision problems, and neuromuscular pain, suggest that neuronal complications comprise a crucial component of COVID-19 pathobiology. A growing body of literature indicates that SARS-CoV-2 can enter the brain, leading to neuronal defects in COVID-19 patients. Other studies suggest that SARS-CoV-2 may aggravate neuronal complications due to its effects on the cerebrovascular system. Emerging pieces of evidence show that stroke can be one of the leading neurological complications in COVID-19. In this review, we describe the observations about neuronal complications of COVID-19 and how SARS-CoV-2 may invade the brain. We will also discuss the cerebrovascular problems and occurrence of stroke in COVID-19 patients. We will also present the observations and our views about the potential pharmacological strategies and targets in COVID-19. We hope this review will help comprehend the current knowledge of neuronal and cerebrovascular complications from SARS-CoV-2 infections and highlight the possible long-term consequences of SARS-CoV-2 on the human brain.

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Serum levels of hepcidin and interleukin 6 in Parkinson’s disease

Cited by 21 publications

References 35 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

Mechanisms of Neurodegeneration in Various Forms of Parkinsonism—Similarities and Differences

Neuronal and Cerebrovascular Complications in Coronavirus Disease 2019

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