• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.178-184
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• 2019

Parkinson's disease is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta. In the present study, we investigated whether ${\beta}-Lapachone$ (${\beta}-LAP$), a natural naphthoquinone compound isolated from the lapacho tree (Tabebuia avellanedae), elicits neuroprotective effects in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease mouse model. ${\beta}-LAP$ reduced the tyrosine hydroxylase (TH)-immunoreactive fiber loss induced by MPTP in the dorsolateral striatum, and alleviated motor dysfunction as determined by the rotarod test. In addition, ${\beta}-LAP$ protected against MPTP-induced loss of TH positive neurons, and upregulated B-cell lymphoma 2 protein (Bcl-2) expression in the substantia nigra. Based on previous reports on the neuroprotective role of nuclear factor-E2-related factor-2 (Nrf2) in neurodegenerative diseases, we investigated whether ${\beta}-LAP$ induces upregulation of the Nrf2-hemeoxygenae-1 (HO-1) signaling pathway molecules in MPTP-injected mouse brains. Western blot and immunohistochemical analyses indicated that ${\beta}-LAP$ increased HO-1 expression in glial fibrillary acidic protein-positive astrocytes. Moreover, ${\beta}-LAP$ increased the nuclear translocation and DNA binding activity of Nrf2, and the phosphorylation of upstream adenosine monophosphate-activated protein kinase (AMPK). ${\beta}-LAP$ also increased the localization of p-AMPK and Nrf2 in astrocytes. Collectively, our data suggest that ${\beta}-LAP$ exerts neuroprotective effect in MPTP-injected mice by upregulating the p-AMPK/Nrf2/HO-1 signaling pathways in astrocytes.

• Journal of Microbiology and Biotechnology
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• v.25 no.10
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• pp.1640-1647
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• 2015

We recently reported that the antimicrobial peptide Lumbricusin (NH₂-RNRRWCIDQQA), isolated from the earthworm, increases cell proliferation in neuroblastoma SH-SY5Y cells. Here, we investigated whether Lumbricusin has neurotropic activity in mouse neural stem cells (MNSCs) and a protective effect in a mouse model of Parkinson's disease (PD). In MNSCs isolated from mouse brains, Lumbricusin treatment significantly increased cell proliferation (up to 12%) and reduced the protein expression of p27^Kip1 through proteasomal protein degradation but not transcriptional regulation. Lumbricusin inhibited the 6-OHDA-induced apoptosis of MNSCs, and also showed neuroprotective effects in a mouse PD model, ameliorating the motor impairments seen in the pole, elevated body swing, and rotation tests. These results suggest that the Lumbricusin-induced promotion of neural cell proliferation via p27^Kip1 degradation has a protective effect in an experimental PD model. Thus, the antimicrobial peptide Lumbricusin could possibly be developed as a potential therapeutic agent for the treatment of PD.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.33 no.2
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• pp.27-34
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• 2022

Stimulants, such as amphetamine and methylphenidate, are one of the most effective treatment modalities for attention deficit hyperactivity disorder (ADHD) and may cause various movement disorders. This review discusses various movement disorders related to stimulant use in the treatment of ADHD. We reviewed the current knowledge on various movement disorders that may be related to the therapeutic use of stimulants in patients with ADHD. Recent findings suggest that the use of stimulants and the onset/aggravation of tics are more likely to be coincidental. In rare cases, stimulants may cause stereotypies, chorea, and dyskinesia, in addition to tics. Some epidemiological studies have suggested that stimulants used for the treatment of ADHD may cause Parkinson's disease (PD) after adulthood. However, there is still a lack of evidence that the use of stimulants in patients with ADHD may cause PD, and related studies are only in the early stages. As stimulants are one of the most commonly used medications in children and adolescents, close observations and studies are necessary to assess the effects of stimulants on various movement disorders, including tic disorders and Parkinson's disease.

• The Korean Journal of Rehabilitation Nursing
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• v.13 no.2
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• pp.140-150
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• 2010

Purpose: This study aims to find the factors that affect the degree of self-care performance in Parkinson's disease (PD) patients. Method: This study used a descriptive correlational design. The data were collected using a sample of 80 PD patients, from the university affiliated Parkinson Center in Busan. Pearson's correlations and multiple regression analyses were conducted using the SPSS 18.0. Results: The mean score of the self-care performance was 3.61 (${\pm}0.40$). The highest score observed of self-care performance subscale was medication subscale ($4.55{\pm}0.50$) and the lowest score was observed in the exercise subscale ($3.03{\pm}0.64$). The self-care performance had significant correlations with depression (r=-.32, p<.01), self-care knowledge (r=.28, p<.05), function of motion (r=.25, p<.05), ability of daily activity (r=.22, p<.05), self-efficacy (r=.24, p<.05), and support from medical staff (r=.24, p<.05). The significant predictors of self-care performance included depression (${\beta}=-.28$), status of employment (${\beta}=-.27$), self-care knowledge (${\beta}=-.21$), support from medical staff (${\beta}=-.28$), and educational level (${\beta}=-.28$), accounting for 34% of the variance in the self-care performance. Conclusion: Depression, self-care knowledge, medical support are significant predictors which affect the self-care performance with PD patients.

• Journal of the Korea Convergence Society
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• v.12 no.5
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• pp.39-50
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• 2021

In this study, a meta-analysis was conducted to find out the effects of convergent "untact" exercise programs on the balance, gait, and falls efficacy of Parkinson's patients. In this study, the PICO were Parkinson's disease, virtual reality program and an e-exercise program intervention, a comparative intervention with the contact interventions applied, and without any interventions applied, outcomes were balance, gait, and fall efficacy. The survey period was between January and February 2021, and five papers were selected and subjected to meta-analysis. Risk of bias, a tool commonly used for randomized control trial studies, was used. Furthermore, RevMan program was used to investigate effect size of untact exercise programs. The result of the meta-analysis showed that the effect size of balance of the untact exercise program group was 1.27 (SMD=1.27; 95% CI 0.72 to 1.83) (Z=4.51, p<0.001), the effect size of fall efficacy was 0.52 (SMD=0.52; 95% CI -0.000 to 1.03) (Z=1.96, p=0.05), and the effect size of gait was -0.40 (SMD=-0.40; 95% CI -1.00 to 0.10)(Z=1.32, p>0.05). A total of 5 literature analysis showed that untact exercise program is more effective in improving balance and falls efficacy than contact exercise program, but no difference in effectiveness was shown on gait.

• Journal of Sasang Constitutional Medicine
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• v.27 no.2
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• pp.270-287
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• 2015

Objectives To evaluate the neuroprotective effects of modified Yuldahanso-tang (MYH) in a Parkinson's disease mouse model. Methods 1) Four groups (each of 8 rats per group) were used in this study. 2) The neuroprotective effect of MYH was examined in a Parkinson's disease mouse model. C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg/day), intraperitoneal (i.p.) for 5 days. 3) The brains of 2 mice per group were removed and frozen at $-20^{\circ}C$, and the striatum-substantia nigra part was seperated. The protein volume was measured by Bradford method following Bio-Rad protein analyzing kit. Using mouse/Rat Dopamine ELISA Assay Kit. 4) The brains of 2 mice per group were separated and removed. TH-immunohistochemical was examined in the MPTP-induced Parkinson's disease mice to evaluate the neuroprotective effects of MYH on ST and SNpc. 5) Two mice out of each group were anesthetized and skulls were opened from occipital to frontal direction to take out the brains. The brains added TTC solution for 20 minutes for staining. 6) The water tank used for morris water maze test was filled with $28^{\circ}C$ water, and a round platform of 10cm in diameter was installed for mice to step on. The study was carried out once a day within 30 seconds, keep exercising to step on the platform in the pool. 7) The brains of two mice out of each group were fixed in 10% formaldehyde solution and paraphillin substance was infiltrated. They were fragmented by microtome, and observed under an optical microscope after Hematoxylin & Eosin staining. 8) A round acrylic cylinder with its upper side open was filled with clean water and depressive mouse models were forced to swim for 15 minutes. After 24 hours the animals were put in the same equipment for 5 minutes and were forced to swim. 9) The convenient, simple, and accurate high-performance liquid chromatography (HPLC) method was established for simultaneous determination of Neurotransmitters in MPTP-MYH group. Results 1) MYH possess Dopamine cell protective effect on MPTP-induced injury in striatum and substantia nigra pars compacta. 2) MYH inhibits the loss of tyrosine hydroxylase-immunoreacitive (TH-IR) cells in the striatum and substantia nigra pars compacta on MPTP-induced injury in C57BL/6 mice. 3) MYH possesses improvement effect on MPTP-induced memory deterioration in C57BL/6 mice through the reduction of prolongated Sort of lost time by MPTP injection using the Morris water maze test. 4) MYH possesses hippocampal neuron protective effect on MPTP-induced injury in C57BL/6 mice. 5) MYH possesses improvement effect on MPTP-induced motor behaviour deficits and depression in C57BL/6 mice through the reduction of prolongated losing motion by MPTP injection using the Forced swimming test. 6) MYH increases serotonin product amount on MPTP-induced injury in C57BL/6 mice. Conclusions This experiment suggests that the neuroprotective effect of MYH is mediated by the increase in Dopamin, TH-ir cell, Hippocampus and Serotonin. Furthermore, MYH essential oil may serve as a potential preventive or therapeutic agent regarding Parkinson's disease.

• The Journal of the Society of Stroke on Korean Medicine
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• v.8 no.1
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• pp.34-39
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• 2007

Objective : To report cases of patients with Parkinson's syndrome. Design : Case-series Patients and methods : 35 of patients with Parkinson's syndrome who visited Department of Cardiovascular and Neurologic Diseases of Kyunghee Oriental Medical Center were treated by acupuncture and herbal medicine from May until December 2007. 35 patients were participated in this study. 21 patients were dropped out during the trial, and we evaluated symptom progress of 14 patients by using several questionnaires such as Unified Parkinson's Disease Rating Scale(UPDRS), modified Hoehn & Yahr stage (H&Y stage) and Schwab & England ADL scale(S&E ADL scale). Results : The whole group consists of 14 male patients and 21 female patients. Mean±SD age range is 64.5±8.4. There were no significant differences of the demographic and clinical characteristics between the case group and drop-out group. The mean±SD medical treatment period of the Case group were 8.4±6.3weeks, the mean±SD of the total score in first medical treatment UPDRS section 1~3 were 29.6±11.0, the mean±SD of the final score were 27.1±12.6, all of which showed significant improvement(p=0.007). There were no significant changes on the H&Y stage and S&E ADL scale. Conclusion : Patients with Parkinson's syndrome who visited Department of Cardiovascular and Neurologic diseases of Kyunghee Oriental Medical Center had a tendency of showing improvement in clinical symptoms.

• Biomolecules & Therapeutics
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• v.27 no.5
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• pp.442-449
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• 2019

This study sought to evaluate the effects of Asiatic acid in LPS-induced BV2 microglia cells and 1-methyl-4-phenyl-pyridine ($MPP^+$)-induced SH-SY5Y cells, to investigate the potential anti-inflammatory mechanisms of Asiatic acid in Parkinson's disease (PD). SH-SY5Y cells were induced using $MPP^+$ to establish as an in vitro model of PD, so that the effects of Asiatic acid on dopaminergic neurons could be examined. The NLRP3 inflammasome was activated in BV2 microglia cells to explore potential mechanisms for the neuroprotective effects of Asiatic acid. We showed that Asiatic acid reduced intracellular production of mitochondrial reactive oxygen species and altered the mitochondrial membrane potential to regulate mitochondrial dysfunction, and suppressed the NLRP3 inflammasome in microglia cells. We additionally found that treatment with Asiatic acid directly improved SH-SY5Y cell viability and mitochondrial dysfunction induced by $MPP^+$. These data demonstrate that Asiatic acid both inhibits the activation of the NLRP3 inflammasome by downregulating mitochondrial reactive oxygen species directly to protect dopaminergic neurons from, and improves mitochondrial dysfunction in SH-SY5Y cells, which were established as a model of Parkinson's disease. Our finding reveals that Asiatic acid protects dopaminergic neurons from neuroinflammation by suppressing NLRP3 inflammasome activation in microglia cells as well as protecting dopaminergic neurons directly. This suggests a promising clinical use of Asiatic acid for PD therapy.

• Korean Journal of Exercise Nutrition
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• v.23 no.4
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• pp.26-31
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• 2019

[Purpose] Numerous epidemiological studies have shown that it is possible to prescribe exercise for neurodegenerative disease, such as Alzheimer's disease and Parkinson's disease. However, despite the availability of diverse scientific knowledge, the effects of exercise in this regard are still unclear. Therefore, this study attempted to investigate a substance, such as black chokeberry (Aronia melanocapa L.) that could improve the ability of the treatment and enhance the benefits of exercising in neurodegenerative diseases. [Methods] The cell viability was tested with 2,3-bis[2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolim-5-carboxanilide and the cells were stained with ethidium homodimer-1 solution. The mRNA expression levels were evaluated by microarray. The active compounds of black chokeberry ethanolic extract (BCE) were analyzed by gas chromatography. The chemical shift analysis in the brain was performed using magnetic resonance spectroscopy. [Results] BCE treatment decreased hydrogen peroxide-induced L6 cell death and beta amyloid induced primary neuronal cell death. Furthermore, BCE treatment significantly reduced the mRNA levels of the inflammatory factors, such as IL-1α, Cxcl13, IL36rn, Itgb2, Epha2, Slamf8, Itgb6, Kdm6b, Acvr1, Cd6, Adora3, Cd27, Gata3, Tnfrsf25, Cd40lg, Clec10a, and Slc11a1, in the primary neuronal cells. Next, we identified 16 active compounds from BCE, including D-mannitol. In vivo, BCE (administered orally at a dosage of 50 mg/kg) significantly regulated chemical shift in the brain. [Conclusion] Our findings suggest that BCE can serve as a candidate for neurodegenerative disease therapy owing to its cyto-protective and anti-inflammatory effects. Therefore, BCE treatment is expected to prevent damage to the muscles and neurons of the athletes who continue high intensity exercise. In future studies, it would be necessary to elucidate the effects of combined BCE intake and exercise.

• Korean Journal of Clinical Pharmacy
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• v.28 no.4
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• pp.285-292
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• 2018

Background: Long-term levodopa therapy relieves the motor dysfunction associated with Parkinson's disease (PD), but has various effects on non-motor symptoms, including cognitive dysfunction, hallucinations, and affective disorders, and can exacerbate certain aspects of dementia-like cognitive dysfunction. Here, we investigated the relationship between levodopa treatment and development of dementia in patients with PD. Methods: This retrospective study analyzed 76 consecutive patients with PD who had taken levodopa between 2011 and 2015. The participants were initially free of dementia and had initial daily levodopa doses of below 600 mg. Patients who did and did not develop comorbid dementia were compared in terms of potential predictor variables, including PD onset age, sex, levodopa doses, and non-dementia comorbidities. Results: Of the 76 patients, 21 (27.6%) developed dementia, which was followed by hallucinations and insomnia. The independent predictors of incident dementia were PD onset age and second-year and third-year average levodopa doses that were higher than the first-year average levodopa dose. Patients who developed dementia had significantly higher average daily levodopa doses and levodopa dose increases over the 6-year treatment period than those who did not develop dementia. In addition, patients with higher levodopa doses were more likely to experience hallucinations. Conclusion: These results suggest that increases in levodopa doses may be associated with a greater risk of cognitive impairment in patients with PD. Therefore, motor and cognitive functions and levodopa dose increases should be evaluated regularly during long-term levodopa therapy in patients with PD.