scholarly journals Activated Schwann cells and increased inflammatory cytokines IL‐1β, IL‐6, and TNF‐α in patients' sural nerve are lack of tight relationship with specific sensory disturbances in Parkinson's disease

2019 ◽  
Vol 26 (5) ◽  
pp. 518-526 ◽  
Author(s):  
Hui Zhang ◽  
Jing Wu ◽  
Fei‐Fei Shen ◽  
Yong‐Sheng Yuan ◽  
Xiao Li ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Schwann Cells ◽  
Inflammatory Cytokines ◽  
Sural Nerve ◽  
Tnf Α ◽  
Sensory Disturbances

scholarly journals Effects of anesthetic method on inflammatory response in patients with Parkinson’s disease: a randomized controlled study

2020 ◽  
Author(s):  
Won Jung Hwang ◽  
Min Ah Joo ◽  
Jin Joo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
General Anesthesia ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Surgical Stress ◽  
Neutrophil Migration ◽  
Controlled Study ◽  
Group I ◽  
Tnf Α

Abstract BackgroundThe pathogenesis of Parkinson’s disease (PD) involves degeneration of dopaminergic neurons, which is influenced by innate and adaptive immunity. IL-17 is a characteristic cytokine secreted by Th17 cells, which acts as a powerful stimulator of neutrophil migration and infiltration and promotes the secretion of inflammatory cytokines. General anesthesia and surgical stress induce immune and inflammatory responses that activate the immunosuppressive mechanism in the perioperative period. The present study investigated changes in levels of inflammatory cytokines, such as IL-17, IL-1β, and TNF-α, in patients with PD undergoing general anesthesia with inhalational anesthetics or TIVA.MethodsAdult patients, aged 40–75 years, scheduled for cerebral stimulator implantation were enrolled. Upon arrival at the operating theater, patients were allocated to the inhalational (I) or TIVA (T) group using block randomization. In group I, anesthesia was induced by tracheal intubation 1–2 min after intravenous administration of propofol (1–2 mg/kg) and rocuronium (0.6–1 mg/kg). Thereafter, anesthesia was maintained with 1–2 vol% sevoflurane, 0.01–0.2 kg/min remifentanil, and O2/air (FiO2 0.4). In group T, propofol (3–6 µg/mL), remifentanil (2–6 ng/mL), and rocuronium (0.6–1 mg/kg) were administered using target controlled infusion (TCI) for induction of anesthesia. Blood samples were obtained preoperatively (T0), 2 h after induction of anesthesia (T1), and 24 h after surgery (T2). IL-17, IL-1β, and TNF-α levels were evaluated by ELISA.ResultsSerum levels of IL-17 were elevated at T2 in group I compared to group T but the difference was not statistically significant. IL-1β tended to be greater in group I compared to group T, but the differences were not significant. (Fig. 3). TNF-α was slightly higher at all time points in group T and showed a tendency to increase at T2 in both groups, but this was not statistically significant (Fig. 4).ConclusionsTIVA may be useful for inhibiting neuroinflammation by inhibiting the increase in serum levels of IL-17 24 h after implantation surgery. Serum IL-17 level may be used as a biomarker for PD progression.TRIAL REGISTRATION:Clinical Research Information Service of Korea National Institute of Health (CRIS) Identification number: KCT0002061. Registered 25 October 2019 - Retrospectively registered, https://cris.nih.go.kr/cris/search/search_result_st01.jsp?seq=15125

scholarly journals Qigong Exercise May Reduce Serum TNF-α Levels and Improve Sleep in People with Parkinson’s Disease: A Pilot Study

Medicines ◽  
2017 ◽  
Vol 4 (2) ◽  
pp. 23 ◽  
Author(s):  
Sanghee Moon ◽  
Marshall Schmidt ◽  
Irina Smirnova ◽  
Yvonne Colgrove ◽  
Wen Liu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Pilot Study ◽  
Tnf Α

scholarly journals Implantation of autologous peripheral nerve grafts into the substantia nigra of subjects with idiopathic Parkinson's disease treated with bilateral STN DBS: a report of safety and feasibility

2017 ◽  
Vol 126 (4) ◽  
pp. 1140-1147 ◽  
Author(s):  
Craig G. van Horne ◽  
Jorge E. Quintero ◽  
Julie A. Gurwell ◽  
Renee P. Wagner ◽  
John T. Slevin ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Peripheral Nerve ◽  
Neurotrophic Factors ◽  
Sural Nerve ◽  
Cell Function ◽  
Nerve Graft ◽  
Clinical Trial Registration ◽  
Peripheral Nerve Graft

OBJECTIVE One avenue of intense efforts to treat Parkinson's disease (PD) involves the delivery of neurotrophic factors to restore dopaminergic cell function. A source of neurotrophic factors that could be used is the Schwann cell from the peripheral nervous system. The authors have begun an open-label safety study to examine the safety and feasibility of implanting an autologous peripheral nerve graft into the substantia nigra of PD patients undergoing deep brain stimulation (DBS) surgery. METHODS Multistage DBS surgery targeting the subthalamic nucleus was performed using standard procedures in 8 study participants. After the DBS leads were implanted, a section of sural nerve containing Schwann cells was excised and unilaterally delivered into the area of the substantia nigra. Adverse events were continuously monitored. RESULTS Eight of 8 participants were implanted with DBS systems and grafts. Adverse event profiles were comparable to those of standard DBS surgery. Postoperative MR images did not reveal edema, hemorrhage, or significant signal changes in the graft target region. Three participants reported a patch of numbness on the outside of the foot below the sural nerve harvest site. CONCLUSIONS Based on the safety outcome of the procedure, targeted peripheral nerve graft delivery to the substantia nigra at the time of DBS surgery is feasible and may provide a means to deliver neurorestorative therapy. Clinical trial registration no.: NCT01833364 (clinicaltrials.gov)

scholarly journals Ageing and MPTP-sensitivity depend on molecular and ultrastructural signatures of Astroglia and Microglia in mice nigra

2020 ◽  
Author(s):  
PL Abhilash ◽  
Upasna Bharti ◽  
Haorei Yarreiphang ◽  
Mariamma Philip ◽  
Rashmi Santhosh Kumar ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Old Age ◽  
Middle Age ◽  
Strain Differences ◽  
Experimental Models ◽  
Data Availability ◽  
Specific Distribution ◽  
Tnf Α ◽  
Objective Evidence

ABSTRACTGlia show region-specific distribution in CNS and often mal-adapt to age-associated alterations in their niche. Some studies on autopsied nigra of Parkinson’s disease (PD) patients and experimental models propose gliosis as a putative trigger of neuronal loss. Epidemiological studies propose an ethnic bias in PD prevalence, as Caucasians are more susceptible than non-whites. Similarly, different mice strains are variably sensitive to MPTP. We had earlier likened divergent MPTP-sensitivity of C57BL/6J and CD-1 mice with differential susceptibility to PD based on differences in neuronal numbers.Here we examined whether the variability was also incumbent to inter-strain differences in glial features. Stereological counts showed more microglia and fewer astrocytes in the nigra of MPTP-susceptible normal C57BL/6J mice, suggesting persistence of an immune-vigilant state. Pronounced MPTP-induced microgliosis and astrogliosis in both strains suggest glial involvement in pathogenesis. ELISA-based estimation of pro-inflammatory cytokines in the ventral midbrain revealed middle-age specific augmentation of TNF-α and IL-6 that reduced at old-age, suggesting middle-age as a critical, inflamm-aging associated time-point. IL-1β levels declined gradually. Inter-strain differences in TNF-α, including that seen post-MPTP, persisted across ageing while IL-6 and IL-1β showed upregulation at old-age. Levels of anti-inflammatory cytokine TGF-β were higher in CD-1. The enzymes MAO-A, MAO-B and iNOS were upregulated in both strains upon MPTP-challenge. Enhancement in fracktalkine and hemeoxygenase-1, post-MPTP, may be neuronal compensatory signals. Most importantly, ultrastructural observations of elongated glial mitochondria vis-à-vis the shrunken ones in neurons, suggest upscaling of glial functions with neurotoxic consequences. Thus, glia could be key modulators of ageing and disease-susceptibility.Significance statementPeople of Caucasians ancestry are more susceptible to Parkinson’s disease, than the Asians, for reasons not completely understood. Surprisingly, their admixed population “the Anglo-Indians” that lives in India; are much less prone. We designed a disease model around two different laboratory mice i.e. C57BL/6 and CD-1 mice and extrapolated the results to the ethnicities, using a neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP). Our study provides objective evidence that astroglia are inherently more and microglia fewer in the mice that resist MPTP. They secret low levels of neuroinflammatory proteins and their gut microbiota is typical. The glial mitochondria may hold the key to cure neurodegeneration.Data availability statementThe data that support the findings of this study are available from the corresponding author upon request.

scholarly journals PD-1 Knockout Aggravates Motor Dysfunction In The MPTP Model of Parkinson's Disease By Inducing Microglial Activation And Neuroinflammation In Mice

2021 ◽  
Author(s):  
Ying-Ying Cheng ◽  
Bei-Yu Chen ◽  
Gan-Lan Bian ◽  
Yin-Xiu Ding ◽  
Liang-Wei CHEN
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Microglial Activation ◽  
Cell Activation ◽  
Microglial Cell ◽  
Motor Dysfunction ◽  
Glial Cell Activation ◽  
Tnf Α ◽  
Regulation Mechanisms ◽  
Mptp Model

Abstract Background: Abundant microglial reaction and neuroinflammation are typical pathogenetic hallmark of brains in Parkinson’s disease (PD) patients, but regulation mechanisms are poorly understood. In this study, the promoting effects of PD-1-difficiency on microglial activation, neuroinflammation and motor dysfunction were identified using PD animal model.Methods: Using C57 wild-type (WT), PD-1 knockout (KO) and MPTP model, we designed WT-control, KO-control, WT-MPTP and KO-MPTP groups. Motor dysfunction of animal, distribution of PD-1-positive cells, dopaminergic neuronal survival, glial cell activation and generation of inflammatory cytokines in midbrains were observed by behavior detection, immunohistochemistry and western blot methods. Results: Microglial cells showing PD-1/Iba1 double-positivity were numerously distributed in the substantia nigra of control whereas they decreased in MPTP model. Compared with WT-MPTP, KO-MPTP mice exacerbated in their motor dysfunction, decreased level of TH expression and decreased TH-positive neuronal protrusions. Microglial cell activation and expression of proinflammatory cytokine iNOS, TNF-α, IL-1β and IL-6 significantly increased, and levels and phosphorylation of AKT and ERK1/2 were also elevated in KO-MPTP mice. Conclusions: PD-1 knockout could aggravate motor dysfunction of MPTP mouse model by promoting microglial activation and neuroinflammation in midbrains, suggesting that PD-1 signaling abnormality might be involved in PD pathogenesis or progression.

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