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Parkinson Disease: HELP
Articles from Tokyo
Based on 520 articles published since 2008
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These are the 520 published articles about Parkinson Disease that originated from Tokyo during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
1 Editorial Editorial and introduction: Behavioral aspects of Parkinson's disease. 2017

Friedman, Joseph H / Bhidayasiri, Roongroj / Truong, Daniel D. ·Butler Hospital, Department of Neurology, Alpert Medical School of Brown University, RI, USA. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok 10330, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Truong Neuroscience Institute, Parkinson's and Movement Disorders Institute, Orange Coast Memorial Medical Center, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28087061.

ABSTRACT: -- No abstract --

2 Editorial Nonmotor symptoms in Parkinson's disease: are we still waiting for the honeymoon? 2016

Colosimo, C / Bhidayasiri, R. ·Department of Neurology, Santa Maria University Hospital, Terni, Italy. carlo.colosimo@uniroma1.it. · Department of Medicine, Faculty of Medicine, Chulalongkorn Center of Excellence for Parkinson's Disease and Related Disorders, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand. · Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. ·Eur J Neurol · Pubmed #27611181.

ABSTRACT: -- No abstract --

3 Editorial What is NODDI and what is its role in Parkinson's assessment? 2016

Kamagata, Koji / Hatano, Taku / Aoki, Shigeki. ·b Department of Radiology , Juntendo University Graduate School of Medicine , Bunkyo-ku , Tokyo , Japan. · a Department of Neurology , Juntendo University Graduate School of Medicine , Bunkyo-ku , Tokyo , Japan. ·Expert Rev Neurother · Pubmed #26777076.

ABSTRACT: -- No abstract --

4 Editorial Familial Parkinson's disease/parkinsonism. 2015

Tomiyama, Hiroyuki / Lesage, Suzanne / Tan, Eng-King / Jeon, Beom S. ·Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan. · Sorbonne Universités, UPMC Université Paris 6 UMRS 1127, Inserm U 1127, CNRS UMR 7225, Institut du Cerveau et de la Moelle Épinière (ICM), Paris, France. · Department of Neurology, Singapore General Hospital and Neuroscience & Behavioral Disorders Program, Duke-NUS Graduate Medical School, National Neuroscience Institute, Singapore. · Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea. ·Biomed Res Int · Pubmed #25961036.

ABSTRACT: -- No abstract --

5 Review Regulation of membrane dynamics by Parkinson's disease-associated genes. 2018

Inoshita, Tsuyoshi / Cui, Changxu / Hattori, Nobutaka / Imai, Yuzuru. ·Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan. yzimai@juntendo.ac.jp. ·J Genet · Pubmed #30027905.

ABSTRACT: Parkinson's disease (PD), the second most common neurodegenerative disease after Alzheimer's disease, develops sporadically, and its cause is unknown. However, 5-10% of PD cases are inherited as monogenic diseases, which provides a chance to understand the molecular mechanisms underlying neurodegeneration. Over 20 causative genes have already been identified and are being characterized. These PD-associated genes are broadly classified into two groups: genes involved in mitochondrial functions and genes related to membrane dynamics such as intracellular vesicle transport and the lysosomal pathway. In this review, we summarize the latest findings on the mechanism by which members of the latter group of PD-associated genes regulate membrane dynamics, and we discuss how mutations of these genes lead to dopaminergic neurodegeneration.

6 Review Peripheral and central autonomic nervous system: does the sympathetic or parasympathetic nervous system bear the brunt of the pathology during the course of sporadic PD? 2018

Orimo, Satoshi / Ghebremedhin, Estifanos / Gelpi, Ellen. ·Department of Neurology, Kanto Central Hospital, 6-25-1 Kami-Yoga, Setagaya-ku, Tokyo, 158-8531, Japan. orimo@kanto-ctr-hsp.com. · Institute of Clinical Neuroanatomy, J. W. Goethe-University, Theodor-Stern-Kai 7, 60590, Frankfurt/Main, Germany. · Neurological Tissue Bank of the Biobank-Hospital Clinic-IDIBAPS, Barcelona, Spain. · Institute of Neurology, Medical University of Vienna, Vienna, Austria. ·Cell Tissue Res · Pubmed #29869180.

ABSTRACT: It is a well-established fact that the sympathetic, parasympathetic and enteric nervous systems are affected at early stages in Parkinson's disease (PD). However, it is not yet clarified whether the earliest pathological events preferentially occur in any of these three divisions of the autonomic nervous system (ANS). Significant involvement of the peripheral autonomic nervous system of the heart and gastrointestinal tract has been documented in PD. Accumulating evidence suggests that the PD pathology spreads centripetally from the peripheral to central nervous system through autonomic nerve fibers, implicating the ANS as a major culprit in PD pathogenesis and a potential target for therapy. This study begins with a brief overview of the structures of the central and peripheral autonomic nervous system and then outlines the major clinicopathological manifestations of cardiovascular and gastrointestinal disturbances in PD.

7 Review [Voxel-Based Morphometry and Social Cognitive Function in Parkinson's Disease]. 2017

Kobayakawa, Mutsutaka. ·Department of Informatics, Faculty of Informatics, Tokyo University of Information Sciences. ·Brain Nerve · Pubmed #29172197.

ABSTRACT: In recent years, voxel-based morphometry (VBM) has been increasingly used to investigate local brain structures in Parkinson's disease (PD). Compared to healthy participants, PD patients tend to show reduced brain volume in limbic and paralimbic areas in early disease stages, while the neocortical areas, such as the temporal and frontal cortices, are affected in advanced patients. Moreover, there are many studies showing correlation between cognitive performance and local brain volume. In the last decade, emotional and social cognitive function, such as facial emotion recognition, emotional decision-making, and theory of mind, have been the target of VBM analysis in PD. These studies facilitate understanding of the nature of communication and behavioral disorders that some PD patients display. However, there are discrepancies in VBM results between studies. Future studies need to employ larger sample sizes and combined analysis of brain perfusion or network connectivity in order to confirm brain structural changes and their effects on social cognitive function in PD patients.

8 Review Lysosomal defects in ATP13A2 and GBA associated familial Parkinson's disease. 2017

Sato, Shigeto / Li, Yuanzhe / Hattori, Nobutaka. ·Department of Neurology, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. · Research Institute for Diseases of Old Age, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan. · Department of Neurology, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. nhattori@juntendo.ac.jp. ·J Neural Transm (Vienna) · Pubmed #28894968.

ABSTRACT: Genes encoding lysosomal proteins, such as ATP13A2 and GBA, are associated with familial Parkinson's disease (PD). Heterozygous mutations in GBA are strongly associated with familial PD. ATP13A2, which encodes a lysosomal P-type ATPase, has been identified as the causative gene for Kufor-Rakeb syndrome. While lysosomal dysfunction due to these mutations exhibited early onset Parkinsonism, each animal model demonstrated different pathological mechanisms. Clinicogenetic and animal model studies recently identified several lysosomal alterations that play a role in the pathogenesis of PD.

9 Review The Oligomer Hypothesis in α-Synucleinopathy. 2017

Ono, Kenjiro. ·Department of Neurology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan. onoken@med.showa-u.ac.jp. ·Neurochem Res · Pubmed #28828740.

ABSTRACT: Lewy bodies and Lewy neurites in the brain constitute the main histopathological features of Parkinson's disease (PD) and dementia with Lewy bodies. They comprise amyloid-like fibrils composed of α-synuclein (αS), a small protein (~14 kDa). Because the aggregation of αS in the brain has been implicated as a critical step in the development of these diseases, the research for disease-modifying drugs has focused on modification of the αS aggregation process in the brain. Recent studies using synthetic αS peptides, a cell culture model, transgenic mice models, and human samples such as cerebrospinal fluids and the blood of PD patients have suggested that pre-fibrillar forms of αS (i.e., oligomers) are more critical than fibrillar forms (such as Lewy bodies) in the pathogenesis of α-synucleinopathies. Based on the accumulating evidence that oligomers play a central role in the pathogenesis of PD and other α-synucleinopathies (the "oligomer hypothesis"). This report reviews the recent findings regarding the oligomer hypothesis in the research of α-synucleinopathies.

10 Review Mitochondrial-Associated Membranes in Parkinson's Disease. 2017

Hattori, Nobutaka / Arano, Taku / Hatano, Taku / Mori, Akio / Imai, Yuzuru. ·Department of Neurology, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo, 113-8421, Japan. nhattori@juntendo.ac.jp. · Department of Neurology, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo, Tokyo, 113-8421, Japan. ·Adv Exp Med Biol · Pubmed #28815529.

ABSTRACT: Parkinson's disease (PD) is a common neurodegenerative disorder, with ageing being a major risk factor. Accordingly, estimates predict an increasing number of PD patients due to our expanding life span. Consequently, developing a true disease-modifying therapy is necessary. In this regard, monogenic PD offers a suitable means for determining pathogenesis. Among monogenic forms of PD, mitochondrial dysfunction may be a major cause and is also likely to be involved in sporadic PD. Thus, mitochondrial impairment may be a common pathway. Recently, mitochondria-associated membranes (MAM) were identified as dynamic sites between mitochondria and endoplasmic reticulum. Indeed, the gene product of α-synuclein is a major component of MAM, with other gene products also involved. This review focuses on the possibility of using MAM as novel therapeutic targets.

11 Review Objective Measurement and Monitoring of Nonmotor Symptoms in Parkinson's Disease. 2017

Klingelhoefer, Lisa / Jitkritsadakul, Onanong / Bhidayasiri, Roongroj. ·Technical University Dresden, Dresden, Germany. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand; Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. ·Int Rev Neurobiol · Pubmed #28802925.

ABSTRACT: The comprehensive evaluation of nonmotor symptoms (NMS) in Parkinson's disease (PD) starts with the awareness of physicians, patients, and caregivers on their nature, clinical presentation, and effect on patient's daily activities and quality of life. This awareness can be better achieved if the symptoms can be visualized, measured, and monitored. As NMS are largely subjective in nature, a majority of them cannot be visualized (unlike tremor, which is easily seen), making their identification and quantification difficult. While symptoms are nonmotor, it does not mean that they are not measurable, as many NMS are integral to motor symptoms of Parkinson's, yet often neglected. In this review, we attempt to provide the most up-to-date and comprehensive literature review on the objective measurement and monitoring of NMS in PD. The aim is to make it clinically relevant by approaching NMS by domains as identified in the NMS Questionnaire. A section on the assessment of nonmotor fluctuations is also included, providing prospects for future objective monitoring. With the advances of technology, it is likely that many NMS will have objective outcomes, thus making these symptoms easily measurable and hopefully lead to future clinical trials that incorporate nonmotor outcomes. Nevertheless, it still requires a physician's judgment to determine which method, scales, objective measures, or monitoring devices or a combination of these is most appropriate to the individual patient in order to answer a particular clinical question.

12 Review Systematic review of hardware-related complications of Deep Brain Stimulation: Do new indications pose an increased risk? 2017

Jitkritsadakul, Onanong / Bhidayasiri, Roongroj / Kalia, Suneil K / Hodaie, Mojgan / Lozano, Andres M / Fasano, Alfonso. ·Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, UHN, Toronto, Ontario, Canada; Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. · Division of Neurosurgery, Department of Surgery, Toronto Western Hospital, University of Toronto, Canada; Krembil Research Institute, Toronto, Ontario, Canada. · Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, UHN, Toronto, Ontario, Canada; Krembil Research Institute, Toronto, Ontario, Canada; Division of Neurology, University of Toronto, Toronto, Ontario, Canada. Electronic address: alfonso.fasano@uhn.ca. ·Brain Stimul · Pubmed #28739219.

ABSTRACT: INTRODUCTION: Deep Brain Stimulation (DBS) is an effective treatment extended broadly to many neurological and psychiatric disorders. Nevertheless, complications may arise during DBS procedures or following implantation due to implanted hardware. This may result in both minor and major adverse events that may necessitate hardware removal and/or compromise maximal therapeutic benefit for the patient. OBJECTIVES AND METHODS: To identify relevant literature on hardware-related complications from DBS procedures by performing a systematic review, and propose how to identify at-risk group and possible preventive approaches. RESULTS: Of 4592 abstract screened, 96 articles fulfilled the selection criteria and were reviewed. Overall, the most common hardware-related complications were infections (5.12% of patients), followed by lead migration (1.60%), fracture or failure of the lead or other parts of the implant (1.46% and 0.73%, respectively), IPG malfunctions (1.06% of patients), and skin erosions without infections (0.48% of patients). New indications for DBS, including Tourette's syndrome, cluster headache, and refractory partial epilepsy, were found to bear a higher incidence of hardware-related infections than established indications such as Parkinson's disease. The highest rate of lead fracture or failure was found in dystonia patients (4.22%). Ultimately, the highest rate of pain at the implantation sites was found in refractory partial epilepsy patients (16.55%). CONCLUSION: Our analysis identified a variety of potential hardware-related complications among patients who underwent DBS procedures. Patients who were at risk of complications, such as patients with dystonia and off-label indications (e.g. Tourette's syndrome) should be informed prior to surgery and closely followed thereafter.

13 Review Parkin mutation may be associated with serious akinesia in a patient with Parkinson's disease. 2017

Uchihara, Yuto / Kataoka, Hiroshi / Yoshino, Hiroyo / Syobatake, Ryogo / Hattori, Nobutaka / Ueno, Satoshi. ·Department of Neurology, Nara Medical University, Kashihara, Nara, Japan. · Department of Neurology, Nara Medical University, Kashihara, Nara, Japan. Electronic address: hk55@naramed-u.ac.jp. · Research Insutitute for Disease of Old Age, Graduated School of Medicine, Juntendo University, Bunkyo-ku, Tokyo, Japan. · Department of Neurology, Graduate School of Medicine, Juntendo University, Bunkyo-ku, Tokyo, Japan. ·J Neurol Sci · Pubmed #28716221.

ABSTRACT: Acute akinesia (AA) is an unusual motor complication in Parkinson's disease (PD). Reported risk factors for AA include infection, trauma, surgical intervention, and the withdrawal of antiparkinsonian medication. Recently, patients with genetic PD were reported to have a three-fold risk of AA than patients with non-genetic PD. We describe a patient with PD associated with a Parkin mutation in whom serious akinesia developed. A 42-year-old man with exon 2 heterozygous deletion and exon 4 heterozygous deletion in the PARK2 gene showed five unexpected AA for several 12h. At fifth AA, he could not move any part of the body while lying in front of a stove in his house all night. He was admitted to our hospital because a third-degree burn had developed on 16% of the body surface area. Parkin mutation in addition to POLG1 or PINK1 mutation may be associated with serious AA.

14 Review A unique glycan-isoform of transferrin in cerebrospinal fluid: A potential diagnostic marker for neurological diseases. 2017

Hoshi, Kyoka / Matsumoto, Yuka / Ito, Hiromi / Saito, Kiyoshi / Honda, Takashi / Yamaguchi, Yoshiki / Hashimoto, Yasuhiro. ·Department of Biochemistry, Fukushima Medical University, 1-Hikarigaoka, Fukushima-City, Fukushima 960-1295, Japan. · Department of Neurosurgery, Fukushima Medical University, 1-Hikarigaoka, Fukushima-City, Fukushima 960-1295, Japan. · Department of Life Science, Fukushima Medical University, 1-Hikarigaoka, Fukushima-City, Fukushima 960-1295, Japan. · Structural Glycobiology Team, Systems Glycobiology Research Group, RIKEN-Max Planck Joint Research Center, RIKEN Global Research Cluster, 2-1 Wako-shi, Saitama 351-0198, Japan. · Department of Biochemistry, Fukushima Medical University, 1-Hikarigaoka, Fukushima-City, Fukushima 960-1295, Japan. Electronic address: yasuc@fmu.ac.jp. ·Biochim Biophys Acta Gen Subj · Pubmed #28711405.

ABSTRACT: BACKGROUND: Cerebrospinal fluid (CSF) is sequestered from blood by the blood-brain barrier and directly communicates with brain parenchymal interstitial fluid, leading to contain specific biomarkers of neurological diseases. SCOPE OF REVIEW: CSF contains glycan isoforms of transferrin (Tf): one appears to be derived from the brain and the other from blood. MAJOR CONCLUSIONS: CSF contains two glycan-isoforms; brain-type Tf and serum-type Tf. Glycan analysis and immunohistochemistry suggest that serum-type Tf having α2, 6sialylated glycans is derived from blood whereas brain-type Tf having GlcNAc-terminated glycans is derived from the choroid plexus, CSF producing tissue. The ratio of serum-type/brain-type Tf differentiates Alzheimer's disease from idiopathic normal pressure hydrocephalus, which is an elderly dementia caused by abnormal metabolism of CSF. The ratios in Parkinson's disease (PD) patients were higher than those of controls and did not appear to be normally distributed. Indeed, detrended normal Quantile-Quantile plot analysis reveals the presence of an independent subgroup showing higher ratios in PD patients. The subgroup of PD shows higher levels of CSF α-synuclein than the rest, indicating that PD includes two subgroups, which differ in levels of brain-type Tf and α-synuclein. GENERAL SIGNIFICANCE: Glycosylation in central nervous system appears to be unique. The unique glycan may be a tag for glycoprotein, which is biosynthesized in the central nervous system. This article is part of a Special Issue entitled Neuro-glycoscience, edited by Kenji Kadomatsu and Hiroshi Kitagawa.

15 Review Focused Ultrasound Treatment, Present and Future. 2017

Abe, Keiichi / Taira, Takaomi. ·Department of Neurosurgery, Tokyo Women's Medical University. ·Neurol Med Chir (Tokyo) · Pubmed #28659546.

ABSTRACT: The discovery that ultrasound waves could be focused inside the skull and heated to high temperatures at a focal point goes back to 1944. However, because the skull causes the ultrasound waves to attenuate and scatter, it was believed that application of this technology would be difficult, and that it would be impossible to use this approach in the surgical treatment of intracranial diseases. Eventually, magnetic resonance image guided focused ultrasound (MRgFUS) surgery began being used to treat uterine fibroids, breast cancer and bone metastasis and locally confined prostate cancer. In the first ten years of the 21st century, new developments in this technology have been achieved, broadening the scope of practical application, and treatment is now being performed in various countries around the world. In 2011, third-generation transcranial focused ultrasound made it possible to use thermocoagulation and create intracranial lesions measuring 2 to 6 mm in diameter with a precision of around 1 mm. It was also possible to produce MR images which relay information of temperature changes in real time, enabling a shift from reversible test heating to irreversible therapeutic heating. This gave rise to the possibility of a minimally-invasive treatment with outcomes similar to those of conventional brain surgery. This method is paving the way to a new future not only in functional neurosurgery, but in cranial neurosurgery targeting conditions such as epilepsy and brain tumors, among others. In this paper, we describe the current state and future outlook of magnetic resonance image guided focused ultrasound, which uses computed tomography (CT) bone images in combination with MRI monitoring of brain temperature.

16 Review A novel function for glucocerebrosidase as a regulator of sterylglucoside metabolism. 2017

Akiyama, Hisako / Hirabayashi, Yoshio. ·Laboratory for Molecular Membrane Neuroscience, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. · Laboratory for Molecular Membrane Neuroscience, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. Electronic address: hirabaya@riken.jp. ·Biochim Biophys Acta Gen Subj · Pubmed #28596107.

ABSTRACT: BACKGROUND: Sterols are major cell membrane lipids, and in many organisms they are modified with glucose to generate sterylglucosides. Glucosylation dramatically changes the functional properties of sterols. The formation of sterylglucosides from sterols in plants, fungi, and bacteria uses UDP-glucose as a glucose donor. By contrast, sterylglucoside biosynthesis in mammals is catalyzed by the transglucosylation activity of glucocerebrosidases, with glucosylceramide acting as the glucose donor. Recent success in isolation and structural determination of sterylglucosides in the vertebrate central nervous system shows that transglucosylation also occurs in vivo. These analyses also revealed that sterylglucoside aglycons are composed of several cholesterol-related metabolites, including a plant-type sitosteryl. SCOPE OF REVIEW: In this review, we discuss the biological functions and metabolism of sterylglucosides. We also summarize new findings from studies on the metabolism of vertebrate sterylglucosides and review the circumstances underlying the recent discovery of sterylglucosides in vertebrate brain. Finally, we discuss the role of sterylglucosides in a variety of neurodegenerative disorders such as Gaucher disease and Parkinson's disease. MAJOR CONCLUSIONS: The biological significance of UDP-glucose-independent sterol glucosylation is still unknown, but it is plausible that glucosylation may provide sterols with novel biological functions. Even though sterol glucosylation is a simple reaction, it can dramatically change the physical properties of sterols. GENERAL SIGNIFICANCE: Sterylglucosides may play roles in various physiological processes and in the pathogenesis of different diseases. Arriving at a better understanding of them at the organ and cellular level may open up new approaches to developing therapeutics for a variety of diseases. This article is part of a Special Issue entitled Neuro-glycoscience, edited by Kenji Kadomatsu and Hiroshi Kitagawa.

17 Review Clinical Assessments in Parkinson's Disease: Scales and Monitoring. 2017

Bhidayasiri, Roongroj / Martinez-Martin, Pablo. ·Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand; Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · National Center of Epidemiology and CIBERNED, Carlos III Institute of Health, Madrid, Spain. ·Int Rev Neurobiol · Pubmed #28554406.

ABSTRACT: Measurement of disease state is essential in both clinical practice and research in order to assess the severity and progression of a patient's disease status, effect of treatment, and alterations in other relevant factors. Parkinson's disease (PD) is a complex disorder expressed through many motor and nonmotor manifestations, which cause disabilities that can vary both gradually over time or come on suddenly. In addition, there is a wide interpatient variability making the appraisal of the many facets of this disease difficult. Two kinds of measure are used for the evaluation of PD. The first is subjective, inferential, based on rater-based interview and examination or patient self-assessment, and consist of rating scales and questionnaires. These evaluations provide estimations of conceptual, nonobservable factors (e.g., symptoms), usually scored on an ordinal scale. The second type of measure is objective, factual, based on technology-based devices capturing physical characteristics of the pathological phenomena (e.g., sensors to measure the frequency and amplitude of tremor). These instrumental evaluations furnish appraisals with real numbers on an interval scale for which a unit exists. In both categories of measures, a broad variety of tools exist. This chapter aims to present an up-to-date summary of the most relevant characteristics of the most widely used scales, questionnaires, and technological resources currently applied to the assessment of PD. The review concludes that, in our opinion: (1) no assessment methods can substitute the clinical judgment and (2) subjective and objective measures in PD complement each other, each method having strengths and weaknesses.

18 Review Freezing of gait and fall detection in Parkinson's disease using wearable sensors: a systematic review. 2017

Silva de Lima, Ana Lígia / Evers, Luc J W / Hahn, Tim / Bataille, Lauren / Hamilton, Jamie L / Little, Max A / Okuma, Yasuyuki / Bloem, Bastiaan R / Faber, Marjan J. ·Radboud university medical center, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands. ana.silvadelima@radboudumc.nl. · Department of Neurology, Radboud university medical center, Nijmegen, The Netherlands. ana.silvadelima@radboudumc.nl. · CAPES Foundation, Ministry of Education of Brazil, Brasília, DF, Brazil. ana.silvadelima@radboudumc.nl. · Department of Neurology, Radboud university medical center, Nijmegen, The Netherlands. · Michael J Fox Foundation for Parkinson's Research, New York, USA. · Aston University, Birmingham, UK. · Media Lab, Massachusetts Institute of Technology, Cambridge, USA. · Department of Neurology, Juntendo University Shizuoka Hospital, Izunokuni, Shizuoka, Japan. · Radboud university medical center, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands. · Radboud university medical center, Radboud Institute for Health Sciences, Scientific Center for Quality of Healthcare, Nijmegen, The Netherlands. ·J Neurol · Pubmed #28251357.

ABSTRACT: Despite the large number of studies that have investigated the use of wearable sensors to detect gait disturbances such as Freezing of gait (FOG) and falls, there is little consensus regarding appropriate methodologies for how to optimally apply such devices. Here, an overview of the use of wearable systems to assess FOG and falls in Parkinson's disease (PD) and validation performance is presented. A systematic search in the PubMed and Web of Science databases was performed using a group of concept key words. The final search was performed in January 2017, and articles were selected based upon a set of eligibility criteria. In total, 27 articles were selected. Of those, 23 related to FOG and 4 to falls. FOG studies were performed in either laboratory or home settings, with sample sizes ranging from 1 PD up to 48 PD presenting Hoehn and Yahr stage from 2 to 4. The shin was the most common sensor location and accelerometer was the most frequently used sensor type. Validity measures ranged from 73-100% for sensitivity and 67-100% for specificity. Falls and fall risk studies were all home-based, including samples sizes of 1 PD up to 107 PD, mostly using one sensor containing accelerometers, worn at various body locations. Despite the promising validation initiatives reported in these studies, they were all performed in relatively small sample sizes, and there was a significant variability in outcomes measured and results reported. Given these limitations, the validation of sensor-derived assessments of PD features would benefit from more focused research efforts, increased collaboration among researchers, aligning data collection protocols, and sharing data sets.

19 Review [Disease-Modifying Therapy for Parkinson's Disease]. 2017

Shimura, Hideki / Hattori, Nobutaka. ·Department of Neurology, Juntendo University Urayasu Hospital. ·Brain Nerve · Pubmed #28202824.

ABSTRACT: Currently, treatment of Parkinson's disease aims at alleviating its symptoms. However development of disease-modifying drugs has been a remarkable advancement in recent years. Furthermore, clinical trials of immunotherapy against α-synuclein, a protein involved in the pathogenesis of and lesion expansion in Parkinson's disease, have been initiated. Here, the disease-modifying treatment for patients with Parkinson's disease including the current α-synuclein immunotherapy, gene therapy, protein injection therapy, and cell transplantation therapy, has been reviewed.

20 Review The sleeping brain in Parkinson's disease: A focus on REM sleep behaviour disorder and related parasomnias for practicing neurologists. 2017

Bhidayasiri, Roongroj / Sringean, Jirada / Rattanachaisit, Watchara / Truong, Daniel D. ·Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Chulalongkorn Centre of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital and Thai Red Cross Society, Bangkok, Thailand. · Parkinson's and Movement Disorders Institute, Fountain Valley, CA, USA. ·J Neurol Sci · Pubmed #28126342.

ABSTRACT: Sleep disorders are identified as common non-motor symptoms of Parkinson's disease (PD) and recently this recognition has been expanded to include parasomnias, encompassing not only REM sleep behaviour disorder (RBD), but also other non-REM forms. RBD, a prototypical parasomnia in PD, exists even in the prodromal stage of the disease, and is characterized by the presence of dream enactment behaviours occurring alongside a loss of normal skeletal muscle atonia during REM sleep. In contrast, non-REM parasomnias are more frequently observed in the late stage PD. However, the development of these disorders often overlaps and it is not uncommon for PD patients to meet the criteria for more than one type of parasomnias, thus making a clinical distinction challenging for practicing neurologists who are not sleep specialists. Indeed, clinical recognition of the predominant form of parasomnia does not just depend on video-polysomnography, but also on an individual physician's clinical acumen in delineating pertinent clinical history to determine the most likely diagnosis and proceed accordingly. In this review article, we highlight the various forms of parasomnias that have been reported in PD, including, but not limited to, RBD, with a focus on clinical symptomatology and implications for clinical practice. In addition, we review the differences in PD-related parasomnias compared to those seen in general populations. With advances in sleep research and better technology for ambulatory home monitoring, it is likely that many unanswered questions on PD-related parasomnias will soon be resolved resulting in better management of this nocturnal challenge in PD.

21 Review [Deep Brain Stimulation for Parkinson Disease:Mechanisms and New Technology]. 2017

Umemura, Atsushi / Shimo, Yasushi / Iwamuro, Hirokazu / Oyama, Genko / Hattori, Nobutaka / Arai, Hajime. ·Department of Research and Therapeutics for Movement Disorders, Juntendo University Graduate School of Medicine. ·No Shinkei Geka · Pubmed #28100856.

ABSTRACT: -- No abstract --

22 Review Prion-like mechanisms and potential therapeutic targets in neurodegenerative disorders. 2017

Hasegawa, Masato / Nonaka, Takashi / Masuda-Suzukake, Masami. ·Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan. Electronic address: hasegawa-ms@igakuken.or.jp. · Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan. ·Pharmacol Ther · Pubmed #27916654.

ABSTRACT: Prion-like propagation of abnormal intracytoplasmic proteins, which are the defining features of major neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), has been proposed. A growing body of evidence strongly suggests that abnormal tau, α-synuclein and TDP-43 have prion-like properties, convert the corresponding normal proteins into abnormal forms, and are transmitted from cell to cell, spreading throughout the brain. This idea is extremely important not only for understanding the pathogenesis and progression of these diseases, but also for the development of molecular therapies. Since the distributions and spreading of the abnormal proteins are closely associated with disease symptoms and progression, gain-of-toxic-function of these proteins may affect the neurons and glial cells either directly or indirectly, or both. It is essential to regulate the aggregation of abnormal intracellular proteins and their cell-to-cell transmission in order to stop, or at least slow, the progression of these diseases.

23 Review An order in Lewy body disorders: Retrograde degeneration in hyperbranching axons as a fundamental structural template accounting for focal/multifocal Lewy body disease. 2017

Uchihara, Toshiki. ·Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya, Tokyo, Japan. ·Neuropathology · Pubmed #27862327.

ABSTRACT: Initial clinical recognition of "paralysis agitans" by James Parkinson was expanded by Jean-Martin Charcot, who recognized additional clinical findings of his own, such as slowness (distinct from paralysis), rigidity (distinct from spasticity) and characteristic countenance. Charcot assembled these findings under the umbrella of "Parkinson disease (PD)". This purely clinical concept was so prescient and penetrating that subsequent neuropathological and biochemical evidences were ordered along this axis to establish the nigra-central trinity of PD (dopamine depletion, nigral lesion with Lewy bodies: LBs). Although dramatic efficacy of levodopa boosted an enthusiasm for this nigra-centralism, extranigral lesions were identified, especially after identification of alpha-synuclein (αS) as a major constituent of LBs. Frequent αS lesions in the lower brainstem with their presumed upward spread were coupled with the self-propagating property of αS molecule, as a molecular template, to constitute the prion-Braak hypothesis. This hybrid concept might expectedly explain clinical, structural and biochemical features of PD/dementia with Lewy bodies (DLB) as if they were stereotypic. In spite of this ordered explanation, recent studies have demonstrated unexpectedly that αS lesions in the human brain, as well as their corresponding clinical manifestations, are much more disordered. Even with such a chaos of LB disorders, affected neuronal groups are uniformly characterized by hyperbranching axons, which may facilitate distal-dominant degeneration and retrograde progression of LB-related degeneration along axons as a fundamental structural order to template LB disorders. This "structural template" hypothesis may explain why: (i) some selective groups are prone to develop Lewy pathology; (ii) their clinical manifestations (especially non-motor components) are vague and generalized without somatotopic accentuation; (iii) distal axons and terminals are preferentially affected early, which is clinically detectable as reduced myocardial uptake of meta-iodobenzylguanidine in PD/DLB. Because each Lewy-prone system develops LBs independently, their isolated presentation as "focal LB disease" or their whatever combinations as "multifocal LB disease" are a more plausible framework to explain clinicopathological diversities of LB disorders. Clinical criteria are now being revised to integrate these clinicopathological disorders of PD/DLB. To gain closer access to the reality of the human brain, it is necessary to facilitate more interactions between clinicopathological and experimental fields so that both are mutually critical and complementary for improved diagnosis and treatment.

24 Review Neurotransmitter release: vacuolar ATPase V0 sector c-subunits in possible gene or cell therapies for Parkinson's, Alzheimer's, and psychiatric diseases. 2017

Higashida, Haruhiro / Yokoyama, Shigeru / Tsuji, Chiharu / Muramatsu, Shin-Ichi. ·Kanazawa University Research Center for Child Mental Development, Kanazawa, 920-8640, Japan. haruhiro@med.kanazawa-u.ac.jp. · Kanazawa University Research Center for Child Mental Development, Kanazawa, 920-8640, Japan. · Division of Neurology, Department of Medicine, Jichi Medical University, Tochigi, 329-0498, Japan. · Center for Gene and Cell Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan. ·J Physiol Sci · Pubmed #27289535.

ABSTRACT: We overview the 16-kDa proteolipid mediatophore, the transmembrane c-subunit of the V0 sector of the vacuolar proton ATPase (ATP6V0C) that was shown to mediate the secretion of acetylcholine. Acetylcholine, serotonin, and dopamine (DA) are released from cell soma and/or dendrites if ATP6V0C is expressed in cultured cells. Adeno-associated viral vector-mediated gene transfer of ATP6V0C into the caudate putamen enhanced the depolarization-induced overflow of endogenous DA in Parkinson-model mice. Motor impairment was ameliorated in hemiparkinsonian model mice when ATP6V0C was expressed with DA-synthesizing enzymes. The review discusses application in the future as a potential tool for gene therapy, cell transplantation therapy, and inducible pluripotent stem cell therapy in neurological diseases, from the view point of recent findings regarding vacuolar ATPase.

25 Review Understanding the role of the Parkinson's disease nurse specialist in the delivery of apomorphine therpy. 2016

Bhidayasiri, Roongroj / Boonpang, Kamolwan / Jitkritsadakul, Onanong / Calne, Susan M / Henriksen, Tove / Trump, Sally / Chaiwong, Suchapit / Susang, Phenprapa / Boonrod, Nonglak / Sringean, Jirada / van Laar, Teus / Drent, Martje / Chaudhuri, K Ray. ·Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, 10330, Thailand; Department of Rehabilitation Medicine, Juntendo University, Tokyo, Japan. Electronic address: rbh@chulapd.org. · Chulalongkorn Center of Excellence for Parkinson's Disease & Related Disorders, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, 10330, Thailand. · Pacific Parkinson's Research Center, University of British Columbia, Vancouver, (1982-2007), Canada. · Movement Disorder Clinic, University Hospital of Bispebjerg, Copenhagen, Denmark. · National Parkinson Foundation Centre of Excellence, King's College Hospital, London, United Kingdom. · Department of Neurology, University of Groningen, Groningen, The Netherlands. ·Parkinsonism Relat Disord · Pubmed #27939324.

ABSTRACT: Optimal care of Parkinson's disease (PD) patients should involve a multidisciplinary team (MDT) of which a PD nurse specialist (PDNS) is a key member. The role of a PDNS is particularly prominent in the care of advanced PD patients suitable for apomorphine because, in addition to nursing skills, apomorphine treatment requires liaison, training, interaction and coordination with patients, caregivers and other members of the MDT as well as the interface with primary care physicians. The therapeutic success of apomorphine therapy depends not only upon the pharmacologic drug response, but also on how well the patient understands his/her disease and how to handle the therapy. In this respect, a PDNS is a vital member of the MDT who provides education and training, support, and is available for consultation when problems arise. In this article, we review the literature on the contribution of PDNSs in both continuous subcutaneous apomorphine infusion and intermittent subcutaneous apomorphine injection and highlight the various beneficial aspects of PDNS care, supported by scientific evidence when available. Despite a low level of published evidence, there is strong clinical evidence that the impact of PDNSs on the management of apomorphine therapy is vital and indispensable for the success of this treatment.

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