Levels of serum IL6, TNF-α and sLAG3 are changed and correlated with clinical characteristics in Parkinson’s disease patients: A case-control study

Objective: An increasing body of studies have proved that inflammation plays a crucial role in Parkinson’s disease (PD) pathogenesis. IL-6, TNF-α and sLAG3 are associated with immune disorder. This study aimed to examine the expression of serum IL-6, TNF-α and sLAG3 in PD patients from China. Methods: Forty six PD patients and 42 age and gender-matched healthy controls (HC) were recruited. clinical data, disease assessment scale and serum IL-6, TNF-α and sLAG3 were assessed in PD patients. The levels of inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA). Results: The levels of serum IL-6 and TNF-α were significantly higher in PD patients compared to HC. Serum IL-6 and TNF-α were independent risk factors for PD. The levels of serum sLAG3 and TNF-α were higher in female patients than those of male patients. Significant positive correlation was found between serum TNF-α and H-Y, UPDRS III and HAMA in PD patients. Serum sLAG3 positively correlated with HAMA. Conclusion: Changes in serum inflammatory factors were observed in PD patients, which were correlated with the clinical characteristics. The study supports the previous hypothesis that inflammation is involved in the pathogenesis of PD.

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Serum HMGB1 level is correlated with serum I-FABP level in neonatal patients with necrotizing enterocolitis

BMC Pediatrics ◽

10.1186/s12887-021-02818-6 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ruyahan Huo ◽

Heng Liu ◽

Jing Chen ◽

Hong Sheng ◽

Li Miao

Keyword(s):

Necrotizing Enterocolitis ◽

Clinical Characteristics ◽

Serum Levels ◽

Stage Ii ◽

Inflammatory Factors ◽

Enzyme Linked Immunosorbent Assay ◽

Healthy Controls ◽

Hmgb1 Level ◽

Tnf Α ◽

Significant Difference

Abstract Background This study aims to investigate clinical significance of HMGB1 in neonatal patients with necrotizing enterocolitis (NEC). Methods This observational study enrolled a total of 106 stage II-III NEC neonatal patients, who were admitted in our hospital from March 2014 to March 2019. In addition, 99 suspected NEC patients and 200 healthy controls were included. The serum levels of HMGB1, I-FABP, and inflammatory factors CRP, IL-1β, IL-6 and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). Then, the demographic data and clinical characteristics of all patients were collected. Statistical analysis was conducted to determine the correlation between HMGB1 and the clinical characteristics. Results No significant difference was found in the basic characteristics of NEC patients and healthy controls, except for birth weight and gestational age. The expression levels of HMGB1, I-FABP, and inflammatory factors IL-1β, IL-6 and TNF-α were significantly higher in NEC patients, when compared to healthy controls. The serum levels of HMGB1, I-FABP, IL-1β and IL-6 markedly increased in stage II-III NEC patients, when compared to stage I NEC patients. The Pearson’s analysis revealed a positive correlation between HMGB1 and I-FABP, HMGB1 and IL-1β, and HMGB1 and IL-6. The ROC curve revealed that both HMGB1 and I-FABP can potentially be used as diagnostic factors for NEC. The logistic multivariate regression revealed that I-FABP, IL-1β and IL-6 are independent risk factors for mortality in neonatal NEC patients. Conclusions Serum HMGB1 levels are upregulated in neonatal NEC patients, and these are correlated with the patient’s prognosis.

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Bacoside-A exerts protective effect against Parkinson’s disease-induced functional damage in mice via inhibition of apoptosis and oxidative response

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v19i12.12 ◽

2021 ◽

Vol 19 (12) ◽

pp. 2565-2570

Author(s):

Binbin Zhang ◽

Jiankuan Shi ◽

Lei Chang ◽

Hong Wang ◽

Yaping Wang ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cytochrome C ◽

Parkinson Disease ◽

Protective Effect ◽

Rat Model ◽

Neuronal Degeneration ◽

Inflammatory Factors ◽

Enzyme Linked Immunosorbent Assay ◽

Bacoside A

Purpose: To determine the effect of bacoside-A on Parkinson's disease (PD) in a rat model, and elucidate its mechanism of action.Methods: A rat model of PD was established by administration of 5 µL of 6-hydroxydopamine in ascorbic acid (0.1 %). Measurement of serum levels of inflammatory factors was carried out using enzyme-linked immunosorbent assay (ELISA) kits. Western blotting was used to assay Bax, cytochrome c and Bcl-2 in rat hippocampus.Results: Bacoside-A treatment significantly reduced PD-induced high turning values in rats (p < 0.05). Treatment with bacoside-A reversed PD-mediated suppression of serum activities of CAT and glutathione peroxidase (GPx). In bacoside-A-treated PD rats, dose-dependent suppression of acetylcholinesterase (AChE) and inducible nitric oxide synthase (iNOS) activities were observed (p < 0.05). Bacoside-A-treated PD rats significantly (p < 0.018) reduced interleukin (IL)-1β and IL-6 levels. Treatment of PD rats with bacoside-A effectively reduced levels of tumor necrosis factor (TNF)-α, NF-κB p65, (COX)-2 and p53 protein, and also reversed up-regulations of Bax, cytochrome C, caspase-3 and caspase-9.Conclusion: Bacoside-A exhibits a protective effect against Parkinson disease-induced oxidative damage and neuronal degeneration in rats through downregulation of iNOS, AChE, inflammatory cytokines and pro-apoptotic proteins. Therefore, bacoside-A has potentials for use in the management of Parkinson disease. Keywords: Parkinson disease, Neuroprotective, Pro-apoptotic, Cytokines, Neurotoxicity

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Momordica Charantia Polysaccharides Attenuates MPP+-Induced Injury in Parkinson’s Disease Mice and Cell Models by Regulating TLR4/MyD88/NF-κB Pathway

International Journal of Polymer Science ◽

10.1155/2021/5575636 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Dengjun Guo ◽

Jie Zhou ◽

Meng Zhang ◽

Reyisha Taximaimaiti ◽

Xiaoping Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cytochrome C ◽

Momordica Charantia ◽

Inflammatory Factors ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Cell Models ◽

Activation Effect

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson’s disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-α and IL-1β, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-κB signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all P < 0.05 ), change the metabolic state of neurotransmitters (all P < 0.05 ), induce inflammation (all P < 0.05 ), and induce apoptosis and the occurrence of oxidation reaction (all P < 0.05 ); however, MCPs treatment can significantly reverse the above changes (all P < 0.05 ). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-κB pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-κB pathway.

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Neuroprotective Effects of a GLP-2 Analogue in the MPTP Parkinson’s Disease Mouse Model

Journal of Parkinson s Disease ◽

10.3233/jpd-202318 ◽

2021 ◽

pp. 1-15

Author(s):

Zijuan Zhang ◽

Li Hao ◽

Ming Shi ◽

Ziyang Yu ◽

Simai Shao ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Substantia Nigra ◽

Mouse Model ◽

Neurodegenerative Disorder ◽

Enzyme Linked Immunosorbent Assay ◽

Protective Effects ◽

Neuroprotective Effects ◽

Expression Levels ◽

Dual Agonist

Background: Glucagon-like peptide 2 (GLP-2) is a peptide hormone derived from the proglucagon gene expressed in the intestines, pancreas and brain. Some previous studies showed that GLP-2 improved aging and Alzheimer’s disease related memory impairments. Parkinson’s disease (PD) is a progressive neurodegenerative disorder, and to date, there is no particular medicine reversed PD symptoms effectively. Objective: The aim of this study was to evaluate neuroprotective effects of a GLP-2 analogue in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) PD mouse model. Methods: In the present study, the protease resistant Gly(2)-GLP-2 (50 nmol/kg ip.) analogue has been tested for 14 days by behavioral assessment, transmission electron microscope, immunofluorescence histochemistry, enzyme-linked immunosorbent assay and western blot in an acute PD mouse model induced by MPTP. For comparison, the incretin receptor dual agonist DA5-CH was tested in a separate group. Results: The GLP-2 analogue treatment improved the locomotor and exploratory activity of mice, and improved bradykinesia and movement imbalance of mice. Gly(2)-GLP-2 treatment also protected dopaminergic neurons and restored tyrosine hydroxylase expression levels in the substantia nigra. Gly(2)-GLP-2 furthermore reduced the inflammation response as seen in lower microglia activation, and decreased NLRP3 and interleukin-1β pro-inflammatory cytokine expression levels. In addition, the GLP-2 analogue improved MPTP-induced mitochondrial dysfunction in the substantia nigra. The protective effects were comparable to those of the dual agonist DA5-CH. Conclusion: The present results demonstrate that Gly(2)-GLP-2 can attenuate NLRP3 inflammasome-mediated inflammation and mitochondrial damage in the substantia nigra induced by MPTP, and Gly(2)-GLP-2 shows neuroprotective effects in this PD animal model.

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The Incidence of Parkinson's Disease: A Systematic Review and Meta-Analysis

Neuroepidemiology ◽

10.1159/000445751 ◽

2016 ◽

Vol 46 (4) ◽

pp. 292-300 ◽

Cited By ~ 171

Author(s):

Lauren Hirsch ◽

Nathalie Jette ◽

Alexandra Frolkis ◽

Thomas Steeves ◽

Tamara Pringsheim

Keyword(s):

Systematic Review ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Disorder ◽

Meta Analysis ◽

Age Groups ◽

Significant Heterogeneity ◽

International Studies ◽

Significant Difference ◽

And Gender

Background: Parkinson's disease (PD) is a common neurodegenerative disorder. Epidemiological studies on the incidence of PD are important to better understand the risk factors for PD and determine the condition's natural history. Objective: This systematic review and meta-analysis examine the incidence of PD and its variation by age and gender. Methods: We searched MEDLINE and EMBASE for epidemiologic studies of PD from 2001 to 2014, as a previously published systematic review included studies published until 2001. Data were analyzed separately for age group and gender, and meta-regression was used to determine whether a significant difference was present between groups. Results: Twenty-seven studies were included in the analysis. Meta-analysis of international studies showed rising incidence with age in both men and women. Significant heterogeneity was observed in the 80+ group, which may be explained by methodological differences between studies. While males had a higher incidence of PD in all age groups, this difference was only statistically significant for those in the age range 60-69 and 70-79 (p < 0.05). Conclusion: PD incidence generally increases with age, although it may stabilize in those who are 80+.

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Clinical characteristics of Parkinson's disease in Sudanese patients attending Daoud Charity Clinic in 2020–2021

Journal of the Neurological Sciences ◽

10.1016/j.jns.2021.119594 ◽

2021 ◽

Vol 429 ◽

pp. 119594

Author(s):

Radi Tofaha Alhusseini ◽

Abbasher Hussien ◽

Khabab Mohamed Ahmed ◽

Hussien Abbashar ◽

Amira Abdelgalil ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Clinical Characteristics

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Respiratory changes in Parkinson's disease may be unrelated to dopaminergic dysfunction

Arquivos de Neuro-Psiquiatria ◽

10.1590/s0004-282x2012001100005 ◽

2012 ◽

Vol 70 (11) ◽

pp. 847-851 ◽

Cited By ~ 20

Author(s):

Luciana Ulhôa Guedes ◽

Juliana Melo Rodrigues ◽

Aline Andrioni Fernandes ◽

Francisco E. Cardoso ◽

Verônica Franco Parreira

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Statistical Analysis ◽

Healthy Controls ◽

Maximal Inspiratory Pressure ◽

Age And Gender ◽

Dopaminergic Dysfunction ◽

And Gender ◽

Student’S T ◽

Student’S T Test

OBJECTIVE: To investigate the maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) in patients with Parkinson's disease (PD) during the on and off periods of levodopa and to compare with healthy controls. METHODS: Twenty-six patients were analyzed with Hoehn and Yahr scores (2-3) and 26 age and gender matched-controls. Statistical analysis was performed with Student's t-test for paired and independent samples. RESULTS: MIP and MEP values in patients were significantly lower than the values obtained in controls both for off and on stages -excepted for MIP in women (p=0.28). For patients with PD, the studied parameters did not differ between stages on and off, with the exception of MEP in women (p=0.00). CONCLUSIONS: Patients with PD have respiratory pressure lower than controls, even in early stages of the disease, and dopamine replacement has little impact over these respiratory pressures. These findings suggest that respiratory changes in PD may be unrelated to dopaminergic dysfunction.

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Evaluation of Serum Apolipoprotein E as a Potential Biomarker for Pharmacological Therapeutic Efficacy Monitoring in Dopamine Dictated Disease Spectrum of Schizophrenia and Parkinson’s disease: A Preliminary Study

Journal of Central Nervous System Disease ◽

10.1177/1179573518803585 ◽

2018 ◽

Vol 10 ◽

pp. 117957351880358 ◽

Cited By ~ 1

Author(s):

Ashish Kumar Gupta ◽

Komal Rani ◽

Surabhi Swarnkar ◽

Gaurav Khunger Kumar ◽

Mohd Imran Khan ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Apolipoprotein E ◽

Pharmacological Intervention ◽

Enzyme Linked Immunosorbent Assay ◽

Disease States ◽

Disease Spectrum ◽

Potential Biomarker ◽

Schizophrenic Patients ◽

The Right

Aim of the Study: Parkinson’s disease and schizophrenia are disease end points of dopaminergic deficit and hyperactivity, respectively, in the mid brain. Accordingly, current medications aim to restore normal dopamine levels, overshooting of which results in adverse effects of psychosis and extra-pyramidal symptoms, respectively. There are currently no available laboratory tests to guide treatment decisions or help predict adverse side effects of the drugs. The aim was to therefore explore the possibility of using apolipoprotein E as a biomarker to monitor pharmacological intervention in dopamine dictated states of Parkinson’s disease and schizophrenia for optimum therapy. Methods: Naïve and treated, Parkinson’s disease and schizophrenic patients were recruited from neurology and psychiatry clinics. Serum of healthy volunteers was collected as controls. Serum concentrations of apolipoprotein E was estimated by enzyme-linked immunosorbent assay (ELISA). Pathway analysis was carried out to delineate the interactions of apolipoprotein E in Parkinson’s disease and schizophrenia. Results: Apolipoprotein E levels are higher in Parkinson’s disease patients as compared with schizophrenic samples ( P < .05). Also, post-treatment apolipoprotein E levels in both disease states were at par with levels seen in healthy controls. The interactions of apolipoprotein E validate the results and place the differential expression of the protein in Parkinson’s disease and schizophrenia in the right perspective. Conclusion: Apolipoprotein E concentration across the dopaminergic spectrum suggests that it can be pursued not only as a potential biomarker in schizophrenia and Parkinson’s disease, but can also be an effective tool for clinicians to determine efficacy of drug-based therapy.

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Cerebrospinal Fluid Biomarkers for Kii Amyotrophic Lateral Sclerosis/Parkinsonism-Dementia Complex

Journal of Neurodegenerative Diseases ◽

10.1155/2013/679089 ◽

2013 ◽

Vol 2013 ◽

pp. 1-4

Author(s):

Yui Nakayama ◽

Satoru Morimoto ◽

Misao Yoneda ◽

Shigeki Kuzuhara ◽

Yasumasa Kokubo

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Amyotrophic Lateral Sclerosis ◽

Cerebrospinal Fluid ◽

Enzyme Linked Immunosorbent Assay ◽

Phosphorylated Tau ◽

Total Tau ◽

Lateral Sclerosis

Objective. Amyotrophic lateral sclerosis/parkinsonism-dementia complex is classified as one of the tauopathies. Methods. The total tau, phosphorylated tau, and amyloid β42 levels were assayed in cerebrospinal fluid from patients with Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex (), Alzheimer’s disease (), Parkinson’s disease (), amyotrophic lateral sclerosis (), and controls () using specific enzyme-linked immunosorbent assay methods. Results. Total tau and phosphorylated tau did not increase and amyloid β42 was relatively reduced in Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex. Relatively reduced amyloid β42 might discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from amyotrophic lateral sclerosis and Parkinson’s disease, and the ratios of phosphorylated-tau to amyloid β42 could discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease. Conclusions. Cerebrospinal fluid analysis may be useful to differentiate amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease, amyotrophic lateral sclerosis, and Parkinson’s disease.

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