• 생물정신의학
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• 제24권1호
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• pp.19-25
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• 2017

Previous studies have found that firefighters have a tenfold higher prevalence of Parkinson's disease (PD) compare to the general population. Firefighters are constantly exposed to various occupational hazards including toxic chemicals of fire residue and the toxic chemicals can effects development and progression of PD. Nevertheless, there were no studies about the association between exposure to chemical byproducts of combustion and the development of PD among firefighters. Thus the aim of this study is to look into existing researches regarding the effect of chemical byproducts of combustion on the development of PD. An extensive literature search was conducted to identify harmful chemical components of smoke and fire residue, using the PubMed database during November of 2016. We searched for relevant articles by combining several keywords that contained "Parkinson's disease" and each of the different toxic chemicals, yielding a total of 1401 articles. After applying the selection criteria, 12 articles were chosen. Chemical substances reported to have a harmful effect on PD, in at least one article, were carbon monoxide, toluene, manganese and lead. Carbon monoxide and metal substances including manganese and lead were found to be associated with an increased PD risk in more than two articles. There was a heightened risk of PD in firefighters due to exposure of chemical byproducts of combustion including carbon monoxide, toluene, manganese and lead. However, to the best of our knowledge, to support this result we need more systematic epidemiological studies about these risk factors of PD among firefighters. In addition, further studies for the effects of prolonged exposure to toxic fire residue on the development and progression of PD in firefighters are needed.

• BMB Reports
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• 제43권4호
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• pp.225-232
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• 2010

Parkinson's Disease (PD) is a common neurodegenerative disease characterized by the progressive degeneration of nigrostriatal dopaminergic (DA) neurons. Although the causative factors of PD remain elusive, many studies on PD animal models or humans suggest that glial activation along with neuroinflammatory processes contribute to the initiation or progression of PD. Additionally, several groups have proposed that dysfunction of the blood-brain barrier (BBB) combined with infiltration of peripheral immune cells play important roles in the degeneration of DA neurons. However, these neuroinflammatory events have only been investigated separately, and the issue of whether these phenomena are neuroprotective or neurotoxic remains controversial. We here review the current knowledge regarding the functions of these neuroinflammatory processes in the brain. Finally, we describe therapeutic strategies for the regulation of neuroinflammation with the goal of improving the symptoms of PD.

• 성인간호학회지
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• 제23권4호
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• pp.363-373
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• 2011

Purpose: Fatigue is a common problem in Parkinson's disease (PD), affecting 30~65% of patients with that diagnosis. Only recently has fatigue been recognized as an important clinical feature of PD. The aim of this study was to investigate the level of fatigue and related factors in patients with PD. Methods: Between March 1, and September, 30, 2010, a sample of 181 PD patients agreed to be interviewed. Results: The female patients' PFS (Parkinson Fatigue Scale) score was higher than those of the male patients. Household income and having a Job were significantly correlated with the PFS scores. Among the disease characteristics, motor fluctuations, dyskinesia and modified Hoehn and Yahr stage were significantly correlated with the PFS scores. On stepwise regression analysis, the most important factors related to the PFS scores were depression and sleep disturbance. Conclusion: Fatigue in patients with PD was associated with many factors and strongly associated with depression and sleep disturbance. Fatigue is a multidimensional construct; therefore, multidimensional strategies for relieving specific aspects of fatigue are needed.

• Nutritional Sciences
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• 제9권2호
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• pp.61-67
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• 2006

Green tea has attracted attention with respect to its potential for preventing and treating neurodegenerative disease. The neurotoxin, 6-hydroxydopamine (6-OHDA), was used to produce experimental Parkinson's disease (PD) model. The purpose of this study was to investigate the effects of green tea diet on behavioral changes, striatal dopamine content, and hepatic antioxidant parameters of PD model rats. In this study, we used male Sprague-Dawley rats weighing $200\sim220g$ and injected 6-OHDA into the right substantia nigra and medial forebrain bundle of the brain. The supply of green tea diet was started at 2 weeks before 6-OHDA lesion and continually supplied during 0, 2, and 4 weeks after 6-OHDA lesion (GT-0, GT-2, GT-4). Behavioral disturbance was measured by the stepping and d-amphetamine drug-induced rotation tests. Then, we assayed the striatal dopamine content and the hepatic malondialdehyde (MDA), hydrogen peroxide $(H_2O_2)$, and superoxide dismutase (SOD) activity. The percentage of lesioned forepaw to non-lesioned forepaw step scores was the highest in GT-4 group among all groups at both 3 and 4 weeks after 6-OHDA lesion. At 4 weeks after 6-OHDA lesion, the rotation score was the lowest in GT-2 group (p<0.05). However, increasing rate of the rotation score from 2 to 4 weeks after 6-OHDA lesion was the lowest in GT-4 group. The striatal dopamine content was not significantly different among four groups by green tea diet. The hepatic MDA level was the lowest in GT-4 group among four groups. The hepatic SOD activity was increased with the prolongation of green tea diet period These results suggest that green tea diet affects behavioral changes in rats of PD model. It seems that continuous green tea supplementation has an influence on the reduction of behavioral disturbance and the hepatic MDA level. Accordingly, continuous green tea supplementation was recommended for the prevention and treatment of PD. However, further studies are needed to investigate the mechanisms and efficacy of green tea in PD.

• 한국감성과학회:학술대회논문집
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• 한국감성과학회 2002년도 추계학술대회 논문집
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• pp.140-147
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• 2002

시상은 체감각 정보를 처리하는데 있어서 매우 중요한 역할을 하는 부위이다. 본 연구는 운동장애 환자의 시상에서 뉴론의 활동 특성을 알아보기 위해 수행되었다. 그 결과 체감각으로서의 운동자극에 반응하는 뉴론이 essential tremor (ET) 환자의 nucleus ventralis intermedius (VIM)에서 발견되었다. ET 환자 뉴론의 평균 활동율(firing rate)은 Parkinson's disease (PD) 환자 보다 높았다. 또한 ET 환자의 VIM에서 운동자극에 반응하는 뉴론의 평균 활동율은 PD 환자 보다 높았다. 하지만 촉각자극(touch)에 반응하는 nucleus ventralis caudalis (VC) 뉴론의 활동율은 ET와 PD 집단간에 차가 없었다. Bursting activity를 나타내는 뉴론은 nucleus ventralis oralis anterior (VOP)에서 ET집단이 PD 집단보다 적었다. tremor cell은 VIM에서 PD 보다 ET집단이 더 적었다. 이러한 결과는 체감각 자극에 반응하는 시상 뉴론의 특성이 운동장애의 유형에 따라 서로 다르다는 것을 시사한다.

• BMB Reports
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• 제47권7호
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• pp.369-375
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• 2014

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a pleiotropic bioactive peptide that was first isolated from an ovine hypothalamus in 1989. PACAP belongs to the secretin/glucagon/vasoactive intestinal polypeptide (VIP) superfamily. PACAP is widely distributed in the central and peripheral nervous systems and acts as a neurotransmitter, neuromodulator, and neurotrophic factor via three major receptors (PAC1, VPAC1, and VPAC2). Recent studies have shown a neuroprotective role of PACAP using in vitro and in vivo models. In this review, we briefly summarize the current findings on the neurotrophic and neuroprotective effects of PACAP in different brain injury models, such as cerebral ischemia, Parkinson's disease (PD), and Alzheimer's disease (AD). This review will provide information for the future development of therapeutic strategies in treatment of these neurodegenerative diseases.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.196.2-197
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• 2003

Parkinson's disease (PO) is a widespread neurodegenerative disorder. Even though PD has been studied in many aspects, it is still unknown the molecular signaling mechanisms linking reactive oxygen species (ROS) and neuronal apoptosis in PD. A better understanding of cellular mechanisms that occur in Parkinson's disease is essential for development of new therapies. In this study we investigated the signaling molecules involved in neuronal apoptosis induced by 6-hydroxydopamine (6-OHDA) in human SK-N-SH neuroblastoma cells as a model cellular system. (omitted)

• 한국운동역학회지
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• 제26권3호
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• pp.293-301
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• 2016

Objective: The purpose of this study was to analyze the effects of freezing of gait and visual information on the static postural control ability in patients with Parkinson's Disease (PD) during the bipedal stance with feet together. Method: This study included a total of 36 patients with PD; the freezer group included 17 PD patients (age: $69.3{\pm}6.2yrs$, height: $159.6{\pm}9.0cm$, weight: $63.4{\pm}9.78kg$) and the nonfreezer group included 19 PD patients (age: $71.4{\pm}5.6yrs$, height: $155.8{\pm}7.1cm$, weight: $57.7{\pm}8.6kg$). Static postural control ability was analyzed using variables of center of pressure (COP) and dividing by mediolateral, anteroposterior, and integration factors during a bipedal stance with the eyes open and closed. Results: Freezers and nonfreezers showed increases in anteroposterior velocity, mediolateral velocity, averaged velocity, and mediolateral 95% edge frequency when visual information was blocked. Additionally, freezers had greater anteroposterior range, 95% confidence ellipse area, and COP anteroposterior mean position than nonfreezers. Conclusion: Freezers and nonfreezers showed a reduction in static postural control ability when visual information was blocked. Additionally, the results of this study found a significant difference in static postural control ability between freezers and nonfreezers with PD. In particular, anteroposterior range, 95% confidence ellipse area, and COP anteroposterior mean position might be used to distinguish between freezers and nonfreezers with PD.

• Biomolecules & Therapeutics
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• 제29권6호
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• pp.615-629
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• 2021

An active compound, triterpene saponin, astersaponin I (AKNS-2) was isolated from Aster koraiensis Nakai (AKNS) and the autophagy activation and neuroprotective effect was investigated on in vitro and in vivo Parkinson's disease (PD) models. The autophagy-regulating effect of AKNS-2 was monitored by analyzing the expression of autophagy-related protein markers in SH-SY5Y cells using Western blot and fluorescent protein quenching assays. The neuroprotection of AKNS-2 was tested by using a 1-methyl-4-phenyl-2,3-dihydropyridium ion (MPP⁺)-induced in vitro PD model in SH-SY5Y cells and an MPTP-induced in vivo PD model in mice. The compound-treated SH-SY5Y cells not only showed enhanced microtubule-associated protein 1A/1B-light chain 3-II (LC3-II) and decreased sequestosome 1 (p62) expression but also showed increased phosphorylated extracellular signal-regulated kinases (p-Erk), phosphorylated AMP-activated protein kinase (p-AMPK) and phosphorylated unc-51-like kinase (p-ULK) and decreased phosphorylated mammalian target of rapamycin (p-mTOR) expression. AKNS-2-activated autophagy could be inhibited by the Erk inhibitor U0126 and by AMPK siRNA. In the MPP⁺-induced in vitro PD model, AKNS-2 reversed the reduced cell viability and tyrosine hydroxylase (TH) levels and reduced the induced α-synuclein level. In an MPTP-induced in vivo PD model, AKNS-2 improved mice behavioral performance, and it restored dopamine synthesis and TH and α-synuclein expression in mouse brain tissues. Consistently, AKNS-2 also modulated the expressions of autophagy related markers in mouse brain tissue. Thus, AKNS-2 upregulates autophagy by activating the Erk/mTOR and AMPK/mTOR pathways. AKNS-2 exerts its neuroprotective effect through autophagy activation and may serve as a potential candidate for PD therapy.

• Biomolecules & Therapeutics
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• 제27권1호
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• pp.63-70
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• 2019

Myeloid-derived suppressor cells (MDSCs) that are able to suppress T cell function are a heterogeneous cell population frequently observed in cancer, infection, and autoimmune disease. Immune checkpoint molecules, such as programmed death 1 (PD-1) expressed on T cells and its ligand (PD-L1) expressed on tumor cells or antigen-presenting cells, have received extensive attention in the past decade due to the dramatic effects of their inhibitors in patients with various types of cancer. In the present study, we investigated the expression of PD-1 on MDSCs in bone marrow, spleen, and tumor tissue derived from breast tumor-bearing mice. Our studies demonstrate that PD-1 expression is markedly increased in tumor-infiltrating MDSCs compared to expression in bone marrow and spleens and that it can be induced by LPS that is able to mediate $NF-{\kappa}B$ signaling. Moreover, expression of PD-L1 and CD80 on $PD-1^+$ MDSCs was higher than on $PD-1^-$ MDSCs and proliferation of MDSCs in a tumor microenvironment was more strongly induced in $PD-1^+$ MDSCs than in $PD-1^-$ MDSCs. Although we could not characterize the inducer of PD-1 expression derived from cancer cells, our findings indicate that the study on the mechanism of PD-1 induction in MDSCs is important and necessary for the control of MDSC activity; our results suggest that $PD-1^+$ MDSCs in a tumor microenvironment may induce tumor development and relapse through the modulation of their proliferation and suppressive molecules.