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Parkinson Disease: HELP
Articles from Korea
Based on 1,403 articles published since 2010
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These are the 1403 published articles about Parkinson Disease that originated from Korea during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
26 Review Significant roles of neuroinflammation in Parkinson's disease: therapeutic targets for PD prevention. 2019

Lee, Yujeong / Lee, Seulah / Chang, Seung-Cheol / Lee, Jaewon. ·Department of Pharmacy, College of Pharmacy, Pusan National University, Busan, 46241, Republic of Korea. · Institute of BioPhysio Sensor Technology, Pusan National University, Busan, 46241, Republic of Korea. · Department of Pharmacy, College of Pharmacy, Pusan National University, Busan, 46241, Republic of Korea. neuron@pusan.ac.kr. ·Arch Pharm Res · Pubmed #30830660.

ABSTRACT: Glial cells outnumber neurons in the brain and play important roles in the neuroinflammation that accompanies brain damage in neurodegenerative diseases. In Parkinson's disease (PD), dopaminergic neuronal loss is accompanied by inflammatory changes in microglia, astrocytes, innate immune cells, and infiltrating peripheral immune cells. Neuroinflammation is probably a fundamental immune response to protect neurons from harm and compensate for neuronal damage, but at the same time, its neurotoxic effects exacerbate neuron damage. Furthermore, neuroinflammatory response is regulated by immune cells, such as microglia, astrocytes, and peripheral immune cells, and by cytokines and chemokines. Accordingly, it is crucial that we understand how such immune cells in the brain regulate neuroinflammatory responses in PD pathology. This review describes the roles played by glia-mediated neuroinflammation in PD, both good and bad, and the therapeutic strategies used to treat PD.

27 Review PAK4 signaling in health and disease: defining the PAK4-CREB axis. 2019

Won, So-Yoon / Park, Jung-Jin / Shin, Eun-Young / Kim, Eung-Gook. ·Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, 28644, Korea. · Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, 28644, Korea. eyshin@chungbuk.ac.kr. · Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju, 28644, Korea. egkim@chungbuk.ac.kr. ·Exp Mol Med · Pubmed #30755582.

ABSTRACT: p21-Activated kinase 4 (PAK4), a member of the PAK family, regulates a wide range of cellular functions, including cell adhesion, migration, proliferation, and survival. Dysregulation of its expression and activity thus contributes to the development of diverse pathological conditions. PAK4 plays a pivotal role in cancer progression by accelerating the epithelial-mesenchymal transition, invasion, and metastasis. Therefore, PAK4 is regarded as an attractive therapeutic target in diverse types of cancers, prompting the development of PAK4-specific inhibitors as anticancer drugs; however, these drugs have not yet been successful. PAK4 is essential for embryonic brain development and has a neuroprotective function. A long list of PAK4 effectors has been reported. Recently, the transcription factor CREB has emerged as a novel effector of PAK4. This finding has broad implications for the role of PAK4 in health and disease because CREB-mediated transcriptional reprogramming involves a wide range of genes. In this article, we review the PAK4 signaling pathways involved in prostate cancer, Parkinson's disease, and melanogenesis, focusing in particular on the PAK4-CREB axis.

28 Review Peroxisomal dysfunction in neurodegenerative diseases. 2019

Jo, Doo Sin / Cho, Dong-Hyung. ·School of Life Sciences, Kyungpook National University, 80 Daehakro Bukgu, Daegu, 41566, Republic of Korea. · School of Life Sciences, Kyungpook National University, 80 Daehakro Bukgu, Daegu, 41566, Republic of Korea. dhcho@knu.ac.kr. ·Arch Pharm Res · Pubmed #30739266.

ABSTRACT: Peroxisomes and their (patho-)physiological importance in heath and disease have attracted increasing interest during last few decades. Together with mitochondria, peroxisomes comprise key metabolic platforms for oxidation of various fatty acids and redox regulation. In addition, peroxisomes contribute to bile acid, cholesterol, and plasmalogen biosynthesis. The importance of functional peroxisomes for cellular metabolism is demonstrated by the marked brain and systemic organ abnormalities occuring in peroxisome biogenesis disorders and peroxisomal enzyme deficiencies. Current evidences indicate that peroxisomal function is declined with aging, with peroxisomal dysfunction being linked to early onset of multiple age-related diseases including neurodegenerative diseases. Herein, we review recent progress toward understanding the physiological roles and pathological implications of peroxisomal dysfunctions, focusing on neurodegenerative disease.

29 Review Mitophagy links oxidative stress conditions and neurodegenerative diseases. 2019

Shefa, Ulfuara / Jeong, Na Young / Song, In Ok / Chung, Hyung-Joo / Kim, Dokyoung / Jung, Junyang / Huh, Youngbuhm. ·Department of Biomedical Science, Graduate School, Kyung Hee University, Seoul, South Korea. · Department of Anatomy and Cell Biology, College of Medicine, Dong-A University, Busan, South Korea. · Department of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Cheil General Hospital, Dankook University College of Medicine, Seoul, South Korea. · Department of Anesthesiology and Pain Medicine, College of Medicine, Kosin University, Busan, South Korea. · Department of Biomedical Science, Graduate School; Department of Anatomy and Neurobiology, College of Medicine, Kyung Hee University, Seoul, South Korea. ·Neural Regen Res · Pubmed #30688256.

ABSTRACT: Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases.

30 Review Pathological role of apoptosis signal-regulating kinase 1 in human diseases and its potential as a therapeutic target for cognitive disorders. 2019

Cheon, So Yeong / Cho, Kyoung Joo. ·Anesthesia and Pain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea. · Department of Life Science, College of Science and Engineering, Kyonggi University, 154-42 Gwanggyosan-ro, Yeongtong-gu, Suwon-si, Gyeonggi-do, 16227, Republic of Korea. kcho0611@kgu.ac.kr. ·J Mol Med (Berl) · Pubmed #30617854.

ABSTRACT: Cognitive disorders are among the leading causes of health and social issues, as well as socioeconomic burden. Cognitive dysfunction associated with diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, diabetes, and stroke can lead to dementia. Despite extensive efforts, strategies for the prevention and treatment of cognitive dysfunction are scarce. Apoptosis signal-regulating kinase 1 (ASK1) participates in diverse biological pathological processes, such as cell death, survival, and differentiation, and it has been suggested as a therapeutic target in various diseases. However, the role of ASK1 in cognitive dysfunction has not been clearly examined yet. In addition, only a few studies have reported a possible relationship between ASK1 signaling and cognitive deficits. In this review, we summarized experimental evidences regarding the association between ASK1 and the pathogenesis of various diseases. Furthermore, we reviewed preclinical studies supporting the possibility that ASK1 regulation is a promising target for the prevention/treatment of cognitive disorders. Nevertheless, future studies are necessary to investigate the role of ASK1 in the pathogenic mechanisms underlying cognitive dysfunctions, for the translation of preclinical information into clinical application.

31 Review Disease model organism for Parkinson disease: Drosophila melanogaster. 2019

Aryal, Binod / Lee, Youngseok. ·Department of Bio and Fermentation Convergence Technology, Kookmin University, BK21 PLUS Project, Seoul 02707, Korea. ·BMB Rep · Pubmed #30545438.

ABSTRACT: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. The analyses of their functions and mechanisms have provided important insights into the disease process, which has demonstrated that these factors cause oxidative damage and mitochondrial dysfunction. The most invaluable studies have been performed using disease model organisms, such as mice, fruit flies, and worms. Among them, Drosophila melanogaster has emerged as an excellent model organism to study both environmental and genetic factors and provide insights to the pathways relevant for PD pathogenesis, facilitating development of therapeutic strategies. In this review, we have focused on the fly model organism to summarize recent progress, including pathogenesis, neuroprotective compounds, and newer approaches. [BMB Reports 2019; 52(4): 250-258].

32 Review Development of Multifunctional Molecules as Potential Therapeutic Candidates for Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis in the Last Decade. 2019

Savelieff, Masha G / Nam, Geewoo / Kang, Juhye / Lee, Hyuck Jin / Lee, Misun / Lim, Mi Hee. ·SciGency Science Communications , Ann Arbor , Michigan 48104 , United States. · Department of Chemistry , Ulsan National Institute of Science and Technology (UNIST) , Ulsan 44919 , Republic of Korea. · Department of Chemistry , Korea Advanced Institute of Science and Technology (KAIST) , Daejeon 34141 , Republic of Korea. ·Chem Rev · Pubmed #30095897.

ABSTRACT: Neurodegenerative diseases pose a substantial socioeconomic burden on society. Unfortunately, the aging world population and lack of effective cures foreshadow a negative outlook. Although a large amount of research has been dedicated to elucidating the pathologies of neurodegenerative diseases, their principal causes remain elusive. Metal ion dyshomeostasis, proteopathy, oxidative stress, and neurotransmitter deficiencies are pathological features shared across multiple neurodegenerative disorders. In addition, these factors are proposed to be interrelated upon disease progression. Thus, the development of multifunctional compounds capable of simultaneously interacting with several pathological components has been suggested as a solution to undertake the complex pathologies of neurodegenerative diseases. In this review, we outline and discuss possible therapeutic targets in Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis and molecules, previously designed or discovered as potential drug candidates for these disorders with emphasis on multifunctionality. In addition, underrepresented areas of research are discussed to indicate new directions.

33 Review Toward Exosome-Based Neuronal Diagnostic Devices. 2018

Yoo, Yong Kyoung / Lee, Junwoo / Kim, Hyungsuk / Hwang, Kyo Seon / Yoon, Dae Sung / Lee, Jeong Hoon. ·Department of Electrical Engineering, Kwangwoon University, 447-1 Wolgye, Nowon, Seoul 01897, Korea. yongkyoung0108@gmail.com. · Department of Electrical Engineering, Kwangwoon University, 447-1 Wolgye, Nowon, Seoul 01897, Korea. mindsjw@gmail.com. · Department of Electrical Engineering, Kwangwoon University, 447-1 Wolgye, Nowon, Seoul 01897, Korea. hskim@kw.ac.kr. · Department of Clinical Pharmacology and Therapeutics, College of Medicine, Kyung Hee University, Seoul 02447, Korea. k.hwang@khu.ac.kr. · School of Biomedical Engineering, Korea University, Seoul 02841, Korea. dsyoon@korea.ac.kr. · Department of Electrical Engineering, Kwangwoon University, 447-1 Wolgye, Nowon, Seoul 01897, Korea. jhlee@kw.ac.kr. ·Micromachines (Basel) · Pubmed #30501125.

ABSTRACT: Targeting exosome for liquid biopsy has gained significant attention for its diagnostic and therapeutic potential. For detecting neuronal disease diagnosis such as Alzheimer's disease (AD), the main technique for identifying AD still relies on positron-emission tomography (PET) imaging to detect the presence of amyloid-β (Aβ). While the detection of Aβ in cerebrospinal fluid has also been suggested as a marker for AD, the lack of quantitative measurements has compromised existing assays. In cerebrospinal fluid, in addition to Aβ, T-Tau, and P-Tau, alpha-synuclein has been considered a biomarker of neurodegeneration. This review suggests that and explains how the exosome can be used as a neuronal diagnostic component. To this end, we summarize current progress in exosome preparation/isolation and quantification techniques and comment on the outlooks for neuronal exosome-based diagnostic techniques.

34 Review Psychiatric Manifestation in Patients with Parkinson's Disease. 2018

Han, Ji Won / Ahn, Yebin D / Kim, Won-Seok / Shin, Cheol Min / Jeong, Seong Jin / Song, Yoo Sung / Bae, Yun Jung / Kim, Jong-Min. ·Department of Neuropsychiatry, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Rehabilitation Medicine, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Urology, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Nuclear Medicine, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Radiology, Seoul National University Bundang Hospital, Seongnam, Korea. · Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Korea. ·J Korean Med Sci · Pubmed #30450025.

ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative disorder. Although its major manifestation is motor symptoms, resulting from the loss of dopaminergic neurons in the substantia nigra, psychiatric symptoms, such as depression, anxiety, hallucination, delusion, apathy and anhedonia, impulsive and compulsive behaviors, and cognitive dysfunction, may also manifest in most patients with PD. Given that the quality of life - and the need for institutionalization - is so highly dependent on the psychiatric well-being of patients with PD, psychiatric symptoms are of high clinical significance. We reviewed the prevalence, risk factors, pathophysiology, and treatment of psychiatric symptoms to get a better understanding of PD for improved management.

35 Review Phytochemical and Pharmacological Role of Liquiritigenin and Isoliquiritigenin From Radix Glycyrrhizae in Human Health and Disease Models. 2018

Ramalingam, Mahesh / Kim, Hyojung / Lee, Yunjong / Lee, Yun-Il. ·Well Aging Research Center, Daegu Gyeongbuk Institute of Science and Technology, Daegu, South Korea. · Division of Pharmacology, Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, South Korea. · Companion Diagnostics and Medical Technology Research Group, Daegu Gyeongbuk Institute of Science and Technology, Daegu, South Korea. ·Front Aging Neurosci · Pubmed #30443212.

ABSTRACT: The increasing lifespan in developed countries results in age-associated chronic diseases. Biological aging is a complex process associated with accumulated cellular damage by environmental or genetic factors with increasing age. Aging results in marked changes in brain structure and function. Age-related neurodegenerative diseases and disorders (NDDs) represent an ever-growing socioeconomic challenge and lead to an overall reduction in quality of life around the world. Alzheimer's disease (AD) and Parkinson's disease (PD) are most common degenerative neurological disorders of the central nervous system (CNS) in aging process. The low levels of acetylcholine and dopamine are major neuropathological feature of NDDs in addition to oxidative stress, intracellular calcium ion imbalance, mitochondrial dysfunction, ubiquitin-proteasome system impairment and endoplasmic reticulum stress. Current treatments minimally influence these diseases and are ineffective in curing the multifunctional pathological mechanisms. Synthetic neuroprotective agents sometimes have negative reactions as an adverse effect in humans. Recently, numerous ethnobotanical studies have reported that herbal medicines for the treatment or prevention of NDDs are significantly better than synthetic drug treatment. Medicinal herbs have traditionally been used around the world for centuries. Radix Glycyrrhizae (RG) is the dried roots and rhizomes of

36 Review Magnetic Resonance-Guided Focused Ultrasound in Neurosurgery: Taking Lessons from the Past to Inform the Future. 2018

Jung, Na Young / Chang, Jin Woo. ·Department of Neurosurgery, Brain Research Institute, Yonsei University College of Medicine, Seoul, Korea. ·J Korean Med Sci · Pubmed #30369860.

ABSTRACT: Magnetic resonance-guided focused ultrasound (MRgFUS) is a new emerging neurosurgical procedure applied in a wide range of clinical fields. It can generate high-intensity energy at the focal zone in deep body areas without requiring incision of soft tissues. Although the effectiveness of the focused ultrasound technique had not been recognized because of the skull being a main barrier in the transmission of acoustic energy, the development of hemispheric distribution of ultrasound transducer phased arrays has solved this issue and enabled the performance of true transcranial procedures. Advanced imaging technologies such as magnetic resonance thermometry could enhance the safety of MRgFUS. The current clinical applications of MRgFUS in neurosurgery involve stereotactic ablative treatments for patients with essential tremor, Parkinson's disease, obsessive-compulsive disorder, major depressive disorder, or neuropathic pain. Other potential treatment candidates being examined in ongoing clinical trials include brain tumors, Alzheimer's disease, and epilepsy, based on MRgFUS abilities of thermal ablation and opening the blood-brain barrier. With the development of ultrasound technology to overcome the limitations, MRgFUS is gradually expanding the therapeutic field for intractable neurological disorders and serving as a trail for a promising future in noninvasive and safe neurosurgical care.

37 Review Non-cell-autonomous actions of α-synuclein: Implications in glial synucleinopathies. 2018

Lim, Somin / Kim, Han-Joon / Kim, Dong-Kyu / Lee, Seung-Jae. ·Department of Biomedical Sciences and Medicine, Neuroscience Research Institute, Seoul National University College of Medicine, Seoul 03080, Republic of Korea. · Department of Neurology, Seoul National University Hospital, Seoul 03080, Republic of Korea. · Department of Biomedical Sciences and Medicine, Neuroscience Research Institute, Seoul National University College of Medicine, Seoul 03080, Republic of Korea. Electronic address: sjlee66@snu.ac.kr. ·Prog Neurobiol · Pubmed #30173732.

ABSTRACT: Many neurodegenerative diseases are derived from the combined consequences of genetic and environmental factors. One of the common features implicated in the neurodegenerative processes is aggregation of disease-specific neuronal proteins. These proteins are accumulated not only directly in neurons, but also indirectly involve glial cells. Whereas the focus of research has been directed towards the impacts of protein aggregation upon neurons, the influence that it exerts on glial cells has been relatively overlooked. Recent studies, however, provide strong evidence on pathogenic responses of glial cells originated from the neuron-derived protein aggregates. Here, we critically examine the latest advancement in investigating how glial cells are activated in neurodegenerative disorders that are associated with α-synuclein aggregates. Often referred to as synucleinopathies, these include Parkinson disease, dementia with Lewy bodies, and multiple system atrophy. To further illustrate, we would discuss paracrine actions of α-synuclein aggregates secreted from neuronal cells in promoting pathogenic reactions from various types of glia and evaluate the non-cell-autonomous mechanism compared to a cell-autonomous one. Such analyses of the impacts of glial responses in neurodegenerative diseases, in the long term, could be further utilized in developing different treatments of the diseases and potentially discovering new drugs.

38 Review Abnormal hippocampal neurogenesis in Parkinson's disease: relevance to a new therapeutic target for depression with Parkinson's disease. 2018

Lim, Juhee / Bang, Yeojin / Choi, Hyun Jin. ·College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam-si, Gyeonggi-do, 13488, Republic of Korea. · College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam-si, Gyeonggi-do, 13488, Republic of Korea. hjchoi3@cha.ac.kr. ·Arch Pharm Res · Pubmed #30136247.

ABSTRACT: Parkinson's disease (PD) is a common progressive neurodegenerative disorder characterized by motor dysfunction, including bradykinesia, tremor, rigidity, and postural instability. Recent clinical findings recognize PD as a complex disease with diverse neuropsychiatric complications. Depression is the most frequent non-motor psychiatric symptom experienced in PD, and it is associated with poor quality of life. While the pathophysiology of PD-associated depression is not directly related to neurodegenerative processes in the substantia nigra, underlying mechanisms remain unclear and there are few symptomatic treatments. Altered adult hippocampal neurogenesis is considered crucial for the development and treatment of depression. In genetic animal models and human postmortem studies of PD, severely impaired adult neurogenesis has been observed, with patients showing hippocampal atrophy and disrupted hippocampal neurogenesis. Because adult newborn neurons appear to exert various functions, which relate to non-motor symptoms observed in PD, there might be a close correlation between malformation of newborn neurons in the adult hippocampus and depressive symptoms. Here, we discuss current concepts regarding impaired hippocampal neurogenesis and non-motor symptoms of PD, and review PD-associated pathophysiological factors regulating neurogenesis, including inflammatory signaling and autophagy. We present a novel framework for targeting adult hippocampal neurogenesis, which could provide a promising treatment for PD-associated depression.

39 Review Cellular phenotypes as inflammatory mediators in Parkinson's disease: Interventional targets and role of natural products. 2018

Jiang, Xu / Ganesan, Palanivel / Rengarajan, Thamaraiselvan / Choi, Dong-Kug / Arulselvan, Palanisamy. ·Department of Neurology, Shenzhen Shajing Affiliated Hospital of Guangzhou Medical University, 3 Shajing St, Baoan Qu, Shenzhen Shi, Guangdong Sheng, 518104, China. Electronic address: dr13510864406@163.com. · Nanotechnology Research Center and Department of Applied Life Science, College of Biomedical and Health Science, Konkuk University, Chungju, 380-701, Republic of Korea; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju, 380-701, Republic of Korea. Electronic address: palanivel67@gmail.com. · Scigen Research and Innovation Pvt. Ltd., Periyar Technology Business Incubator, Periyar Nagar, Thanjavur, 613403, India. Electronic address: thamarairaj2000@gmail.com. · Nanotechnology Research Center and Department of Applied Life Science, College of Biomedical and Health Science, Konkuk University, Chungju, 380-701, Republic of Korea; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju, 380-701, Republic of Korea. Electronic address: choidk@kku.ac.kr. · Scigen Research and Innovation Pvt. Ltd., Periyar Technology Business Incubator, Periyar Nagar, Thanjavur, 613403, India; Muthayammal Centre for Advanced Research, Muthayammal College of Arts and Science, Rasipuram, Namakkal, Tamilnadu, 637408, India. Electronic address: arulbio@gmail.com. ·Biomed Pharmacother · Pubmed #30119171.

ABSTRACT: Pathogenesis of Parkinson's disease (PD) is undoubtedly a multifactorial phenomenon, with diverse etiological agents. Pro-inflammatory mediators act as a skew that directs disease progression during neurodegenerative diseases. Understanding the dynamics of inflammation and inflammatory mediators in preventing or reducing disease progression has recently gained much attention. Inflammatory neuro-degeneration is regulated via cytokines, chemokines, lipid mediators and immune cell subsets; however, individual cellular phenotypes in the Central Nervous System (CNS) acts in diverse ways whose persistent activation leads to unresolving inflammation often causing unfavorable outcomes in neurodegenerative disease like PD. Specifically, activation of cellular phenotypes like astrocytes, microglia, activation of peripheral immune cells requires different activation signals and agents like (cytokines, misfolded protein aggregates, infectious agents, pesticides like organophosphates, etc.,). However, what is unknown is how the different cellular phenotypes respond uniquely and the role of the factors they secrete alters the signal cascades in the complex neuron-microglial connections in the CNS. Hence, understanding the role of cellular phenotypes and the inflammatory mediators, the cross talk among the signals and their receptors can help us to identify the potential therapeutic target using natural products. In this review we have tried to put together the role of cellular phenotypes as a skew that favors PD progression and we have also discussed how the lack of experimental approaches and challenges that affects understanding the cellular targets that can be used against natural derivatives in alleviating PD pathophysiology. Together, this review will provide the better insights into the role of cellular phenotypes of neuroinflammation, inflammatory mediators and the orchestrating factors of inflammation and how they can be targeted in a more specific way that can be used in the clinical management of PD.

40 Review Mechanisms of protein toxicity in neurodegenerative diseases. 2018

Chung, Chang Geon / Lee, Hyosang / Lee, Sung Bae. ·Department of Brain and Cognitive Sciences, DGIST, Daegu, 42988, Republic of Korea. · Department of Brain and Cognitive Sciences, DGIST, Daegu, 42988, Republic of Korea. hyosang22@dgist.ac.kr. · Department of Brain and Cognitive Sciences, DGIST, Daegu, 42988, Republic of Korea. sblee@dgist.ac.kr. ·Cell Mol Life Sci · Pubmed #29947927.

ABSTRACT: Protein toxicity can be defined as all the pathological changes that ensue from accumulation, mis-localization, and/or multimerization of disease-specific proteins. Most neurodegenerative diseases manifest protein toxicity as one of their key pathogenic mechanisms, the details of which remain unclear. By systematically deconstructing the nature of toxic proteins, we aim to elucidate and illuminate some of the key mechanisms of protein toxicity from which therapeutic insights may be drawn. In this review, we focus specifically on protein toxicity from the point of view of various cellular compartments such as the nucleus and the mitochondria. We also discuss the cell-to-cell propagation of toxic disease proteins that complicates the mechanistic understanding of the disease progression as well as the spatiotemporal point at which to therapeutically intervene. Finally, we discuss selective neuronal vulnerability, which still remains largely enigmatic.

41 Review Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States. 2018

Mattson, Mark P / Arumugam, Thiruma V. ·Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: mark.mattson@nih.gov. · Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea. ·Cell Metab · Pubmed #29874566.

ABSTRACT: During aging, the cellular milieu of the brain exhibits tell-tale signs of compromised bioenergetics, impaired adaptive neuroplasticity and resilience, aberrant neuronal network activity, dysregulation of neuronal Ca

42 Review Astrocytes, Microglia, and Parkinson's Disease. 2018

Joe, Eun-Hye / Choi, Dong-Joo / An, Jiawei / Eun, Jin-Hwa / Jou, Ilo / Park, Sangmyun. ·Department of Pharmacology, Ajou University School of Medicine, Suwon 16944, Korea. · Department of Biomedical Sciences, Neuroscience Graduate Program, Ajou University School of Medicine, Suwon 16944, Korea. · Department of Brain Science, Ajou University School of Medicine, Suwon 16944, Korea. · Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon 16944, Korea. ·Exp Neurobiol · Pubmed #29731673.

ABSTRACT: Astrocytes and microglia support well-being and well-function of the brain through diverse functions in both intact and injured brain. For example, astrocytes maintain homeostasis of microenvironment of the brain through up-taking ions and neurotransmitters, and provide growth factors and metabolites for neurons, etc. Microglia keep surveying surroundings, and remove abnormal synapses or respond to injury by isolating injury sites and expressing inflammatory cytokines. Therefore, their loss and/or functional alteration may be directly linked to brain diseases. Since Parkinson's disease (PD)-related genes are expressed in astrocytes and microglia, mutations of these genes may alter the functions of these cells, thereby contributing to disease onset and progression. Here, we review the roles of astrocytes and microglia in intact and injured brain, and discuss how PD genes regulate their functions.

43 Review Non-pharmacological therapies for sleep disturbances in people with Parkinson's disease: A systematic review. 2018

Lee, JuHee / Kim, Yonji / Kim, Yie Lin. ·Mo-Im Kim Nursing Research Institute, College of Nursing, Yonsei University, Seoul, Korea. · Graduate School, College of Nursing, Yonsei University, Seoul, Korea. ·J Adv Nurs · Pubmed #29700848.

ABSTRACT: AIM: To determine the effectiveness of non-pharmacological therapies for sleep disturbances in people with Parkinson's disease (PD). BACKGROUND: Sleep disturbances, which are common in people with PD, may diminish their quality of life. Non-pharmacological therapies are preferred over pharmacological therapies for improving sleep quality, owing to fewer adverse effects. DESIGN: Systematic literature review. DATA SOURCES: A systematic search of eight databases and hand searching was conducted for papers published between 1 January 2000 - 1 January 2016. REVIEW METHODS: The Cochrane methods were followed. Risk of bias was assessed using the Cochrane Collaboration Risk of Bias Tool. RESULTS: Eight studies were identified for data extraction. Therapeutic domains included physical exercise, cognitive behavioural and complementary interventions. Therapies in four of the eight studies significantly improved sleep quality and the unified PD rating scale score. Other studies showed no clear effects on sleep (N = 1), limited effects on sleep (N = 1) or effects in both the intervention and control groups, indicating that the intervention had no distinctive effects (N = 2). CONCLUSIONS: The non-pharmacological intervention types and sleep-related measured outcomes were heterogeneous. Most therapies had inconsistent effects on sleep. The insufficient evidence for non-pharmacological treatments seems related to the unique motor-associated clinical features of PD, which restrict the use of physical exercise therapy, or to individual "wearing-off" periods, which limit group therapy. Further studies on non-pharmacological therapies are required to identify the best interventions for improving sleep quality in people with PD.

44 Review Herbal Prescriptions and Medicinal Herbs for Parkinson-Related Rigidity in Korean Medicine: Identification of Candidates Using Text Mining. 2018

Park, So Hyun / Hwang, Min Seob / Park, Hye Jin / Shin, Hwa Kyoung / Baek, Jin Ung / Choi, Byung Tae. ·1 Division of Humanities and Social Medicine, School of Korean Medicine, Pusan National University , Yangsan, Republic of Korea. · 2 Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University , Yangsan, Republic of Korea. ·J Altern Complement Med · Pubmed #29583014.

ABSTRACT: BACKGROUND: Dongeuibogam (DongYiBaoGian), one of the most important books in Korean medicine, comprises a comprehensive summary of all traditional medicines of North-East Asia before the 17th century. This medicinal literature was mined to establish a list of candidate herbs to treat Parkinson-related rigidity. METHODS: A systematic search for terms describing Parkinson-related rigidity and candidate prescriptions for the treatment of Parkinson-related rigidity in the Dongeuibogam was performed. A high-frequency medicinal herb combination group and candidates for the treatment of Parkinson-related rigidity were also selected through an analysis of medicinal herb combination frequencies. The existing literature pertaining to the potential effects of candidate herbs for Parkinson-related rigidity was reviewed. RESULTS AND CONCLUSIONS: Ten medicinal herb candidates for the treatment of Parkinson-related rigidity were selected, and their respective precedent studies were analyzed.

45 Review Beneficial Effects of Flavonoids Against Parkinson's Disease. 2018

Jung, Un Ju / Kim, Sang Ryong. ·1 Department of Food Science and Nutrition, Pukyong National University , Busan, Korea. · 2 School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Institute of Life Science and Biotechnology, Kyungpook National University , Daegu, Korea. · 3 Brain Science and Engineering Institute, Kyungpook National University , Daegu, Korea. ·J Med Food · Pubmed #29412767.

ABSTRACT: Parkinson's disease (PD) is characterized by the progressive degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta and decreases in striatal dopamine levels. These changes led to several clinical symptoms: rigidity, resting tremor, and bradykinesia. Although the cause of PD remains unclear, it is widely accepted that oxidative stress, neuroinflammation, mitochondrial dysfunction, and insufficient support of neurotrophic factors are involved in the pathophysiology of the disease. However, novel regimens to prevent neurodegeneration and restore the degenerated nigrostriatal DA system are still required. In recent years, there has been a growing interest in naturally occurring phytochemicals, which are believed to reduce the risk of neurodegenerative diseases. This review provides an overview of the scientific literature concerning the preventive and protective roles of flavonoids, one of the largest families of phytochemicals, against PD. In addition to providing antioxidant and anti-inflammatory effects, flavonoids exhibit a neuroprotective effect by activating antiapoptotic pathways that target mitochondrial dysfunction and induce neurotrophic factors. This review suggests that flavonoids may be promising natural products for the prevention of PD and could potentially be utilized as therapeutic compounds against PD, even though there was no report showing that the treatment with flavonoids could restore the aberrant phenotypes of patients with PD.

46 Review Abnormal somatosensory temporal discrimination in Parkinson's disease: Pathophysiological correlates and role in motor control deficits. 2018

Lee, Myung Sik / Lee, Myung Jun / Conte, Antonella / Berardelli, Alfredo. ·Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address: mslee@yuhs.ac. · Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine and Biomedical Research Institute, Busan, Republic of Korea. Electronic address: mslayer9@gmail.com. · Department of Human Neuroscience, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli (IS), Italy. Electronic address: antonella.conte@uniroma1.it. · Department of Human Neuroscience, Sapienza University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli (IS), Italy. Electronic address: alfredo.berardelli@uniroma1.it. ·Clin Neurophysiol · Pubmed #29304419.

ABSTRACT: OBJECTIVE: The somatosensory temporal discrimination threshold (STDT), defined as the shortest time interval required for two tactile stimuli to be perceived as separate, is longer in patients with Parkinson's disease (PD). In this review, we discuss STDT findings in healthy subjects and in PD patients and the relationship between altered STDT and motor disturbances. METHODS: A search was conducted on PubMed for papers dealing with PD and temporal discrimination published from January 1990 to July 2017. RESULTS: Abnormal STDT in PD correlates with disease duration, disease severity and degree of nigrostriatal dopamine loss, and responds to dopaminergic medication. In PD, a prolonged STDT does not correlate, or only marginally correlates, with clinically assessed bradykinesia of finger tapping. By contrast, a prolonged STDT correlates with the variability in amplitude and speed of finger tapping as assessed by means of neurophysiological techniques and may contribute to impaired finger dexterity in PD. CONCLUSIONS: We suggest that abnormal temporal processing of sensory information in PD generates incorrect signals for the execution and control of voluntary movements. SIGNIFICANCE: This review sheds light on unsolved questions regarding the relationship between STDT alterations and motor disturbances in PD and proposes directions for future research on this topic.

47 Review Functional lesional neurosurgery for tremor: back to the future? 2018

Schreglmann, Sebastian R / Krauss, Joachim K / Chang, Jin Woo / Martin, Ernst / Werner, Beat / Bauer, Ronald / Hägele-Link, Stefan / Bhatia, Kailash P / Kägi, Georg. ·Department of Neurology, Kantonsspital St. Gallen, St. Gallen, Switzerland. · Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, London, UK. · Department of Neurosurgery, Medizinische Hochschule Hannover, Hannover, Germany. · Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea. · Center for Focused Ultrasound, University of Zurich, Children's Hospital Zurich, Zurich, Switzerland. · Department of Neurosurgery, Kantonsspital St. Gallen, St. Gallen, Switzerland. ·J Neurol Neurosurg Psychiatry · Pubmed #29269505.

ABSTRACT: For nearly a century, functional neurosurgery has been applied in the treatment of tremor. While deep brain stimulation has been in the focus of academic interest in recent years, the establishment of incisionless technology, such as MRI-guided high-intensity focused ultrasound, has again stirred interest in lesional approaches.In this article, we will discuss the historical development of surgical technique and targets, as well as the technological state-of-the-art of conventional and incisionless interventions for tremor due to Parkinson's disease, essential and dystonic tremor and tremor related to multiple sclerosis (MS) and midbrain lesions. We will also summarise technique-inherent advantages of each technology and compare their lesion characteristics. From this, we identify gaps in the current literature and derive future directions for functional lesional neurosurgery, in particularly potential trial designs, alternative targets and the unsolved problem of bilateral lesional treatment. The results of a systematic review and meta-analysis of the consistency, efficacy and side effect rate of lesional treatments for tremor are presented separately alongside this article.

48 Review Functional dissection of astrocyte-secreted proteins: Implications in brain health and diseases. 2018

Jha, Mithilesh Kumar / Kim, Jong-Heon / Song, Gyun Jee / Lee, Won-Ha / Lee, In-Kyu / Lee, Ho-Won / An, Seong Soo A / Kim, SangYun / Suk, Kyoungho. ·Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea. · Department of Internal Medicine, Division of Endocrinology and Metabolism, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · Department of BioNano Technology, Gachon University, Gyeonggi-do, Republic of Korea. · Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Gyeonggi-do, Republic of Korea. · Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea. Electronic address: ksuk@knu.ac.kr. ·Prog Neurobiol · Pubmed #29247683.

ABSTRACT: Astrocytes, which are homeostatic cells of the central nervous system (CNS), display remarkable heterogeneity in their morphology and function. Besides their physical and metabolic support to neurons, astrocytes modulate the blood-brain barrier, regulate CNS synaptogenesis, guide axon pathfinding, maintain brain homeostasis, affect neuronal development and plasticity, and contribute to diverse neuropathologies via secreted proteins. The identification of astrocytic proteome and secretome profiles has provided new insights into the maintenance of neuronal health and survival, the pathogenesis of brain injury, and neurodegeneration. Recent advances in proteomics research have provided an excellent catalog of astrocyte-secreted proteins. This review categorizes astrocyte-secreted proteins and discusses evidence that astrocytes play a crucial role in neuronal activity and brain function. An in-depth understanding of astrocyte-secreted proteins and their pathways is pivotal for the development of novel strategies for restoring brain homeostasis, limiting brain injury/inflammation, counteracting neurodegeneration, and obtaining functional recovery.

49 Review Understanding the role of glycogen synthase kinase-3 in L-DOPA-induced dyskinesia in Parkinson's disease. 2018

Choi, Hojin / Koh, Seong-Ho. ·a Department of Neurology , Hanyang University College of Medicine , Seoul , South Korea. ·Expert Opin Drug Metab Toxicol · Pubmed #29233065.

ABSTRACT: INTRODUCTION: Levodopa (L-DOPA) is the most commonly used drug for Parkinson's disease (PD), but its long-term use is associated with various complications, including L-DOPA-induced dyskinesia (LID). Many studies have suggested that L-DOPA neurotoxicity and LID are associated with glycogen synthase kinase-3 (GSK-3) activation. Areas covered: LID is caused by striatal dopamine (DA) denervation in PD and pulsatile L-DOPA treatment. These factors lead to dysregulated DA transmission, abnormal intracellular signaling and transcription factors in striatal neurons, and altered gene expression and plasticity at corticostriatal synapses. The mechanisms of L-DOPA toxicity involve oxidative stress, L-DOPA oxidation to quinone, mitochondrial dysfunction, and α-synuclein. GSK-3 has been suggested to play key roles in all the mechanisms associated of L-DOPA toxicity and LID in PD. Expert opinion: GSK-3 plays critical roles in L-DOPA-induced neurotoxicity, and the development of specific methods to inhibit GSK-3 function may help prevent L-DOPA neurotoxicity and LID in PD. However, balanced GSK-3 inhibition and less β-catenin degradation is essential for preventing LID, because too much GSK-3 inhibition increases β-catenin levels, which is related to cancers.

50 Review REM sleep behavior disorder portends poor prognosis in Parkinson's disease: A systematic review. 2018

Kim, Yoon / Kim, Young Eun / Park, Eun Ok / Shin, Chae Won / Kim, Han-Joon / Jeon, Beomseok. ·Department of Neurology, MRC and Movement Disorder Center, Seoul National University Hospital, Parkinson Study Group, Seoul National University College of Medicine, Seoul, South Korea. · Department of Neurology, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, South Korea. · Department of Neurology, Kyung Hee University Medical Center, Seoul, South Korea. · Department of Neurology, MRC and Movement Disorder Center, Seoul National University Hospital, Parkinson Study Group, Seoul National University College of Medicine, Seoul, South Korea. Electronic address: brain@snu.ac.kr. ·J Clin Neurosci · Pubmed #29102236.

ABSTRACT: REM sleep behavior disorder (RBD) is a parasomnia wherein a loss of REM sleep atonia manifests as dream-enactment, often violent. Aside from its significance as a predictor of PD, RBD in PD may imply more than merely screaming at night and experiencing sleep fragmentation. To probe its significance as a prognostic factor in PD, we performed a systematic literature review. Analysis of prospective studies reveals baseline RBD confers a higher risk of developing dementia and hallucinations. In cross-sectional studies, RBD is associated with the non-tremor predominant motor phenotype and autonomic dysfunction. Clinical, imaging, and autopsy studies support the presence of dense and diffuse pathology extending beyond the brainstem in PD with RBD. As RBD in PD is associated with a greater disease burden and an increased risk of mortality, we propose the RBD subtype in PD to highlight that RBD may mark a distinct subtype with relatively poor prognosis.

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