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From articles published in Journal of Movement Disorders during the past two years (2023 ~ ).

Review Articles
Article image
Current Status and Future Perspectives on Stem Cell-Based Therapies for Parkinson’s Disease
Young Cha, Tae-Yoon Park, Pierre Leblanc, Kwang-Soo Kim
J Mov Disord. 2023;16(1):22-41.   Published online January 12, 2023
DOI: https://doi.org/10.14802/jmd.22141
  • 12,180 View
  • 624 Download
  • 21 Web of Science
  • 21 Crossref
AbstractAbstract PDF
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1%–2% of the population over the age of 65. As the population ages, it is anticipated that the burden on society will significantly escalate. Although symptom reduction by currently available pharmacological and/or surgical treatments improves the quality of life of many PD patients, there are no treatments that can slow down, halt, or reverse disease progression. Because the loss of a specific cell type, midbrain dopamine neurons in the substantia nigra, is the main cause of motor dysfunction in PD, it is considered a promising target for cell replacement therapy. Indeed, numerous preclinical and clinical studies using fetal cell transplantation have provided proof of concept that cell replacement therapy may be a viable therapeutic approach for PD. However, the use of human fetal cells remains fraught with controversy due to fundamental ethical, practical, and clinical limitations. Groundbreaking work on human pluripotent stem cells (hPSCs), including human embryonic stem cells and human induced pluripotent stem cells, coupled with extensive basic research in the stem cell field offers promising potential for hPSC-based cell replacement to become a realistic treatment regimen for PD once several major issues can be successfully addressed. In this review, we will discuss the prospects and challenges of hPSC-based cell therapy for PD.

Citations

Citations to this article as recorded by  
  • Nanotechnology in Parkinson’s Disease: overcoming drug delivery challenges and enhancing therapeutic outcomes
    Irfan Ali, Mohammad Adil, Mohammad Imran, Saba Asif Qureshi, Saima Qureshi, Nazeer Hasan, Farhan Jalees Ahmad
    Drug Delivery and Translational Research.2025;[Epub]     CrossRef
  • Emerging Role of Mesenchymal Stromal Cell and Exosome Therapies in Treating Cognitive Impairment
    Vick Key Tew, Muttiah Barathan, Fazlina Nordin, Jia Xian Law, Min Hwei Ng
    Pharmaceutics.2025; 17(3): 284.     CrossRef
  • Advantages and challenges of using allogeneic vs. autologous sources for neuronal cell replacement in Parkinson’s disease: Insights from non-human primate studies
    Marina E. Emborg, Jeanette M. Metzger, Kevin D’Amour, Julia C. Colwell, Lindsey C. Neumann, Ai Zhang, Howard J. Federoff
    Brain Research Bulletin.2025; 224: 111297.     CrossRef
  • Stem Cell-Based Approaches in Parkinson's Disease Research
    Min Seong Kim, Subeen Yoon, Jiwoo Choi, Yong Jun Kim, Gabsang Lee
    International Journal of Stem Cells.2025; 18(1): 21.     CrossRef
  • RNA-based controllers for engineering gene and cell therapies
    Kei Takahashi, Kate E Galloway
    Current Opinion in Biotechnology.2024; 85: 103026.     CrossRef
  • Precision Medicine in Parkinson's Disease Using Induced Pluripotent Stem Cells
    Min Seong Kim, Hyesoo Kim, Gabsang Lee
    Advanced Healthcare Materials.2024;[Epub]     CrossRef
  • A recent update on drugs and alternative approaches for parkinsonism
    Sneha Kispotta, Debajyoti Das, Shakti Ketan Prusty
    Neuropeptides.2024; 104: 102415.     CrossRef
  • Recent Research Trends in Neuroinflammatory and Neurodegenerative Disorders
    Jessica Cohen, Annette Mathew, Kirk D. Dourvetakis, Estella Sanchez-Guerrero, Rajendra P. Pangeni, Narasimman Gurusamy, Kristina K. Aenlle, Geeta Ravindran, Assma Twahir, Dylan Isler, Sara Rukmini Sosa-Garcia, Axel Llizo, Alison C. Bested, Theoharis C. Th
    Cells.2024; 13(6): 511.     CrossRef
  • Continuous immunosuppression is required for suppressing immune responses to xenografts in non-human primate brains
    Su Feng, Ting Zhang, Zhengxiao He, Wenchang Zhang, Yingying Chen, Chunmei Yue, Naihe Jing
    Cell Regeneration.2024;[Epub]     CrossRef
  • The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets
    Alhamdu Adamu, Shuo Li, Fankai Gao, Guofang Xue
    Frontiers in Aging Neuroscience.2024;[Epub]     CrossRef
  • Past, present, and future of cell replacement therapy for parkinson’s disease: a novel emphasis on host immune responses
    Tae-Yoon Park, Jeha Jeon, Young Cha, Kwang-Soo Kim
    Cell Research.2024; 34(7): 479.     CrossRef
  • Dopamine synthesis and transport: current and novel therapeutics for parkinsonisms
    Mary Dayne Sia Tai, Gloria Gamiz-Arco, Aurora Martinez
    Biochemical Society Transactions.2024; 52(3): 1275.     CrossRef
  • Experimental models of Parkinson's disease: Challenges and Opportunities
    Roshan Lal, Aditi singh, Shivam watts, Kanwaljit Chopra
    European Journal of Pharmacology.2024; 980: 176819.     CrossRef
  • The prospective role of mesenchymal stem cells in Parkinson's disease
    Pratima Tambe, Vaishali Undale, Avinash Sanap, Ramesh Bhonde, Nishant Mante
    Parkinsonism & Related Disorders.2024; 127: 107087.     CrossRef
  • Current Landscape of iPSC Haplobanks
    Rubén Escribá, Meral Beksac, Annelise Bennaceur-Griscelli, Joel C. Glover, Satu Koskela, Helen Latsoudis, Sergi Querol, Belén Alvarez-Palomo
    Stem Cell Reviews and Reports.2024; 20(8): 2155.     CrossRef
  • Circuit integration by transplanted human neurons
    Qiang Yuan, Su-Chun Zhang
    Current Opinion in Genetics & Development.2024; 89: 102225.     CrossRef
  • The Abnormal Proliferation of Midbrain Dopamine Cells From Human Pluripotent Stem Cells Is Induced by Exposure to the Tumor Microenvironment
    Jun Xue, Dongyan Wu, Yuting Bao, Yifan Wu, Xin Zhang, Liang Chen
    CNS Neuroscience & Therapeutics.2024;[Epub]     CrossRef
  • Potential for Therapeutic-Loaded Exosomes to Ameliorate the Pathogenic Effects of α-Synuclein in Parkinson’s Disease
    David J. Rademacher
    Biomedicines.2023; 11(4): 1187.     CrossRef
  • Neural Stem Cell Therapies: Promising Treatments for Neurodegenerative Diseases
    Amir Gholamzad, Hadis Sadeghi, Maryam Azizabadi Farahani, Ali Faraji, Mahya Rostami, Sajad Khonche, Shirin Kamrani, Mahsa Khatibi, Omid Moeini, Seyed Armit Hosseini, Mohammadmatin Nourikhani, Mehrdad Gholamzad
    Neurology Letters.2023; 2(2): 55.     CrossRef
  • Should continuous dopaminergic stimulation be a standard of care in advanced Parkinson’s disease?
    Z. Pirtošek, V. Leta, P. Jenner, M. Vérin
    Journal of Neural Transmission.2023; 130(11): 1395.     CrossRef
  • Xeno-free generation of new Yazd human embryonic stem cell lines (Yazd4-7) as a prior stage toward good manufacturing practice of clinical-grade raw materials from discarded embryos: A lab resources report
    Fatemeh Hajizadeh-Tafti, Jalal Golzadeh, Fatemeh Akyash, Somayyeh-Sadat Tahajjodi, Ehsan Farashahi-Yazd, Hassan Heidarian-Meimandi, Behrouz Aflatoonian
    International Journal of Reproductive BioMedicine (IJRM).2023; 21(8): 619.     CrossRef
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Subjective Cognitive Complaints in Cognitively Normal Patients With Parkinson’s Disease: A Systematic Review
Jin Yong Hong, Phil Hyu Lee
J Mov Disord. 2023;16(1):1-12.   Published online November 10, 2022
DOI: https://doi.org/10.14802/jmd.22059
  • 5,458 View
  • 359 Download
  • 14 Web of Science
  • 16 Crossref
AbstractAbstract PDF
Subjective cognitive complaints (SCCs) refer to self-perceived cognitive decline and are related to objective cognitive decline. SCCs in cognitively normal individuals are considered a preclinical sign of subsequent cognitive impairment due to Alzheimer’s disease, and SCCs in cognitively normal patients with Parkinson’s disease (PD) are also gaining attention. The aim of this review was to provide an overview of the current research on SCCs in cognitively normal patients with PD. A systematic search found a lack of consistency in the methodologies used to define and measure SCCs. Although the association between SCCs and objective cognitive performance in cognitively normal patients with PD is controversial, SCCs appear to be predictive of subsequent cognitive decline. These findings support the clinical value of SCCs in cognitively normal status in PD; however, further convincing evidence from biomarker studies is needed to provide a pathophysiological basis for these findings. Additionally, a consensus on the definition and assessment of SCCs is needed for further investigations.

Citations

Citations to this article as recorded by  
  • Cognitive impairment in Parkinson’s disease and other parkinsonian syndromes
    Alexandros Giannakis, Chrissa Sioka, Eugenia Kloufetou, Spiridon Konitsiotis
    Journal of Neural Transmission.2025; 132(3): 341.     CrossRef
  • The Relationship Between Subjective Cognitive Complaints, Invalid Symptom Reporting, and Neurocognitive Test Performance Validity Among Adults Being Evaluated for ADHD
    Matthew S. Phillips, Nataliya Turchmanovych-Hienkel, Mira I. Leese, Brian Ramanauskas, Hannah B. VanLandingham, Christopher Gonzalez, Gabriel P. Ovsiew, Anthony D. Robinson, Brian M. Cerny, Devin M. Ulrich, Jason R. Soble
    Journal of Psychiatric Practice.2025; 31(1): 13.     CrossRef
  • The Multifactorial Memory Questionnaire and Quality of Life: A Longitudinal Study in Parkinson’s Disease
    Emily J. Corti, Natalie Gasson, Hayley Grant, Brayden Wisniewski, Andrea M. Loftus
    Brain Sciences.2025; 15(1): 66.     CrossRef
  • Heterogeneity of cognitive progression and clinical predictors in Parkinson’s disease–subjective cognitive decline
    Jon Rodríguez-Antigüedad, Saül Martínez-Horta, Arnau Puig-Davi, Andrea Horta-Barba, Javier Pagonabarraga, Teresa de Deus Fonticoba, Silvia Jesús, Marina Cosgaya, Juan García Caldentey, María Asunción Ávila-Rivera, Nuria Caballol, Inés Legarda, Jorge Herná
    Journal of Neurology.2025;[Epub]     CrossRef
  • Daily Emotional Experiences in Persons with Parkinson Disease: Relations to Subjective Cognitive Complaints and Quality of Life
    Karen R. Hebert, Mackenzie Feldhacker
    Physical & Occupational Therapy In Geriatrics.2024; 42(3): 228.     CrossRef
  • Subjective Cognitive Complaints in Parkinson's Disease: A Systematic Review and Meta‐Analysis
    Mattia Siciliano, Alessandro Tessitore, Francesca Morgante, Jennifer G. Goldman, Lucia Ricciardi
    Movement Disorders.2024; 39(1): 17.     CrossRef
  • Mild cognitive impairment in Parkinson's disease: current view
    Kurt A. Jellinger
    Frontiers in Cognition.2024;[Epub]     CrossRef
  • Neurocognitive Impairment and Social Cognition in Parkinson’s Disease Patients
    Triantafyllos Doskas, Konstantinos Vadikolias, Konstantinos Ntoskas, George D. Vavougios, Dimitrios Tsiptsios, Polyxeni Stamati, Ioannis Liampas, Vasileios Siokas, Lambros Messinis, Grigorios Nasios, Efthimios Dardiotis
    Neurology International.2024; 16(2): 432.     CrossRef
  • Cognitive disorders in Parkinson's disease
    Victor Kholin, Iryna Karaban, Sergiy Kryzhanovskiy, Nina Karasevich, Natalia Melnik, Maryna Khodakovska, Hanna Shershanova, Natalia Movchun
    Ageing & Longevity.2024; (2 2024): 51.     CrossRef
  • Unveiling the role of subjective cognitive complaints in predicting cognitive impairment in Parkinson´s Disease– A longitudinal study with 4 year of follow up
    Marta Magriço, Bruna Meira, Marco Fernandes, Manuel Salavisa, Marlene Saraiva, Cláudia Borbinha, João Pedro Marto, Raquel Barbosa, Paulo Bugalho
    Neurological Sciences.2024; 45(11): 5271.     CrossRef
  • Self‐ and study partner–reported cognitive decline in older adults without dementia: The role of α‐synuclein and amyloid biomarkers in the Alzheimer's Disease Neuroimaging Initiative
    Kelsey R. Thomas, Katherine J. Bangen, Lindsay J. Rotblatt, Alexandra J. Weigand, Lauren Edwards, Duygu Tosun, Douglas Galasko
    Alzheimer's & Dementia.2024; 20(11): 7777.     CrossRef
  • Mitochondrial Dysfunction in Parkinson’s Disease: A Contribution to Cognitive Impairment?
    Antonella Scorziello, Rossana Sirabella, Maria Josè Sisalli, Michele Tufano, Lucia Giaccio, Elena D’Apolito, Lorenzo Castellano, Lucio Annunziato
    International Journal of Molecular Sciences.2024; 25(21): 11490.     CrossRef
  • Total burden of cerebral small vessel disease predict subjective cognitive decline in patients with Parkinson’s disease
    Wenchao Qiu, Weili Hu, Yingchao Ge, Peiting Liu, Minghui Zhao, Haifeng Lu, Jian Tao, Shouru Xue
    Frontiers in Aging Neuroscience.2024;[Epub]     CrossRef
  • Association of Neuropsychiatric Symptom Profiles With Cognitive Decline in Patients With Parkinson Disease and Mild Cognitive Impairment
    Young-gun Lee, Mincheol Park, Seong Ho Jeong, Kyoungwon Baik, Sungwoo Kang, So Hoon Yoon, Han Kyu Na, Young H. Sohn, Phil Hyu Lee
    Neurology.2023;[Epub]     CrossRef
  • Subjective cognitive complaints in patients with progressive supranuclear palsy
    Jun Seok Lee, Jong Hyeon Ahn, Jong Mok Ha, Jinyoung Youn, Jin Whan Cho
    Frontiers in Neurology.2023;[Epub]     CrossRef
  • Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks
    Kurt A. Jellinger
    International Journal of Molecular Sciences.2023; 25(1): 498.     CrossRef
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Gastrointestinal Dysfunction in Parkinson’s Disease: Neuro-Gastroenterology Perspectives on a Multifaceted Problem
Ai Huey Tan, Kee Huat Chuah, Yuan Ye Beh, Jie Ping Schee, Sanjiv Mahadeva, Shen-Yang Lim
J Mov Disord. 2023;16(2):138-151.   Published online May 24, 2023
DOI: https://doi.org/10.14802/jmd.22220
  • 9,235 View
  • 344 Download
  • 11 Web of Science
  • 11 Crossref
AbstractAbstract PDF
Patients with Parkinson’s disease (PD) face a multitude of gastrointestinal (GI) symptoms, including nausea, bloating, reduced bowel movements, and difficulties with defecation. These symptoms are common and may accumulate during the course of PD but are often under-recognized and challenging to manage. Objective testing can be burdensome to patients and does not correlate well with symptoms. Effective treatment options are limited. Evidence is often based on studies in the general population, and specific evidence in PD is scarce. Upper GI dysfunction may also interfere with the pharmacological treatment of PD motor symptoms, which poses significant management challenges. Several new less invasive assessment tools and novel treatment options have emerged in recent years. The current review provides an overview and a practical approach to recognizing and diagnosing common upper and lower GI problems in PD, e.g., dyspepsia, gastroparesis, small bowel dysfunction, chronic constipation, and defecatory dysfunction. Management aspects are discussed based on the latest evidence from the PD and general populations, with insights for future research pertaining to GI dysfunction in PD.

Citations

Citations to this article as recorded by  
  • Lactiplantibacillus plantarum SG5 inhibits neuroinflammation in MPTP-induced PD mice through GLP-1/PGC-1α pathway
    Yueyan Qi, Yuxuan Dong, Jinhu Chen, Siyou Xie, Xin Ma, Xueping Yu, Yang Yu, Yanqin Wang
    Experimental Neurology.2025; 383: 115001.     CrossRef
  • Leveraging animal models to understand non-motor symptoms of Parkinson's disease
    Thomas Wichmann, Alexandra Nelson, Eileen Ruth S. Torres, Per Svenningsson, Roberta Marongiu
    Neurobiology of Disease.2025; : 106848.     CrossRef
  • Associations between gut microbiota characteristics and non‐motor symptoms following pharmacological and surgical treatments in Parkinson's disease patients
    Agnieszka Gorecka‐Mazur, Anna Krygowska‐Wajs, Agata Furgala, Jiaqi Li, Benjamin Misselwitz, Wojciech Pietraszko, Borys Kwinta, Bahtiyar Yilmaz
    Neurogastroenterology & Motility.2024;[Epub]     CrossRef
  • Clinical diagnosis, prevention, and treatment of neurodyspepsia syndrome using intelligent medicine
    Jingyu Zhu, Wei Meng, Liang Liu, Peixin Hu, Yuling Liang, Wenwen Zhu, Xiaoyan Zhu
    Open Life Sciences.2024;[Epub]     CrossRef
  • Levodopa-induced dyskinesia in Parkinson's disease: Insights from cross-cohort prognostic analysis using machine learning
    Rebecca Ting Jiin Loo, Olena Tsurkalenko, Jochen Klucken, Graziella Mangone, Fouad Khoury, Marie Vidailhet, Jean-Christophe Corvol, Rejko Krüger, Enrico Glaab, Geeta Acharya, Gloria Aguayo, Myriam Alexandre, Muhammad Ali, Wim Ammerlann, Giuseppe Arena, Mi
    Parkinsonism & Related Disorders.2024; 126: 107054.     CrossRef
  • Acupuncture for constipation in Parkinson’s disease: A systematic review and meta-analysis of randomized controlled trials
    Zhao Li, Qun Niu, Kai Yang, Keni Zhao, Shao Yin, Fengya Zhu
    Medicine.2024; 103(29): e38937.     CrossRef
  • Alpha Synuclein Toxicity and Non-Motor Parkinson’s
    Gabriella M. Mazzotta, Carmela Conte
    Cells.2024; 13(15): 1265.     CrossRef
  • Novel strategies in Parkinson’s disease treatment: a review
    Charles L. Mitchell, Dmitry Kurouski
    Frontiers in Molecular Neuroscience.2024;[Epub]     CrossRef
  • Advice to People with Parkinson’s in My Clinic: Probiotics and Prebiotics
    Jia Wei Hor, Tzi Shin Toh, Shen-Yang Lim, Ai Huey Tan
    Journal of Parkinson’s Disease.2024; 14(7): 1507.     CrossRef
  • Unmasking bowel obstruction in a Parkinson’s patient: the influence of cognitive bias in frailty medicine
    Harvey Stevenson, Daniele Ramsay, Waseem Jerjes
    Oxford Medical Case Reports.2024;[Epub]     CrossRef
  • Gastrointestinal Dysfunction Bears on the Clinical‐Biological Profile of Parkinson's Disease
    Jacopo Bissacco, Roberta Bovenzi, Matteo Conti, Clara Simonetta, Davide Mascioli, Rocco Cerroni, Giulia Maria Sancesario, Piergiorgio Grillo, Mariangela Pierantozzi, Alessandro Stefani, Nicola Biagio Mercuri, Marta Camacho, Tommaso Schirinzi
    Movement Disorders Clinical Practice.2024;[Epub]     CrossRef
Article image
GBA1 Variants and Parkinson’s Disease: Paving the Way for Targeted Therapy
Young Eun Huh, Tatiana Usnich, Clemens R. Scherzer, Christine Klein, Sun Ju Chung
J Mov Disord. 2023;16(3):261-278.   Published online June 12, 2023
DOI: https://doi.org/10.14802/jmd.23023
  • 6,618 View
  • 467 Download
  • 7 Web of Science
  • 8 Crossref
AbstractAbstract PDF
Glucosylceramidase beta 1 (GBA1) variants have attracted enormous attention as the most promising and important genetic candidates for precision medicine in Parkinson’s disease (PD). A substantial correlation between GBA1 genotypes and PD phenotypes could inform the prediction of disease progression and promote the development of a preventive intervention for individuals at a higher risk of a worse disease prognosis. Moreover, the GBA1-regulated pathway provides new perspectives on the pathogenesis of PD, such as dysregulated sphingolipid metabolism, impaired protein quality control, and disrupted endoplasmic reticulum-Golgi trafficking. These perspectives have led to the development of novel disease-modifying therapies for PD targeting the GBA1-regulated pathway by repositioning treatment strategies for Gaucher’s disease. This review summarizes the current hypotheses on a mechanistic link between GBA1 variants and PD and possible therapeutic options for modulating GBA1-regulated pathways in PD patients.

Citations

Citations to this article as recorded by  
  • Male sex accelerates cognitive decline in GBA1 Parkinson’s disease
    Silvia Paola Caminiti, Micol Avenali, Alice Galli, Rachele Malito, Giada Cuconato, Caterina Galandra, Rosaria Calabrese, Andrea Pilotto, Alessandro Padovani, Fabio Blandini, Daniela Perani, Cristina Tassorelli, Enza Maria Valente
    npj Parkinson's Disease.2025;[Epub]     CrossRef
  • Classification and Genotype–Phenotype Relationships of GBA1 Variants: MDSGene Systematic Review
    Malco Rossi, Susen Schaake, Tatiana Usnich, Josephine Boehm, Nina Steffen, Nathalie Schell, Clara Krüger, Tuğçe Gül‐Demirkale, Natascha Bahr, Teresa Kleinz, Harutyun Madoev, Björn‐Hergen Laabs, Ziv Gan‐Or, Roy N. Alcalay, Katja Lohmann, Christine Klein
    Movement Disorders.2025;[Epub]     CrossRef
  • Challenges in Gaucher disease: Perspectives from an expert panel
    Gregory A. Grabowski, Priya S. Kishnani, Roy N. Alcalay, S. Grace Prakalapakorn, Barry E. Rosenbloom, Dominick A. Tuason, Neal J. Weinreb
    Molecular Genetics and Metabolism.2025; : 109074.     CrossRef
  • A Comparative Biochemical and Pathological Evaluation of Brain Samples from Knock-In Murine Models of Gaucher Disease
    Makaila L. Furderer, Bahafta Berhe, Tiffany C. Chen, Stephen Wincovitch, Xuntian Jiang, Nahid Tayebi, Ellen Sidransky, Tae-Un Han
    International Journal of Molecular Sciences.2024; 25(3): 1827.     CrossRef
  • Towards a Global View of Parkinson's Disease Genetics
    Marzieh Khani, Catalina Cerquera‐Cleves, Mariam Kekenadze, Peter Wild Crea, Andrew B. Singleton, Sara Bandres‐Ciga
    Annals of Neurology.2024; 95(5): 831.     CrossRef
  • Exploring the Association between Cathepsin B and Parkinson’s Disease
    Changhao Lu, Xinyi Cai, Shilin Zhi, Xiaofen Wen, Jiaxin Shen, Tommaso Ercoli, Elena Rita Simula, Carla Masala, Leonardo A. Sechi, Paolo Solla
    Brain Sciences.2024; 14(5): 482.     CrossRef
  • Clinical, mechanistic, biomarker, and therapeutic advances in GBA1-associated Parkinson’s disease
    Xuxiang Zhang, Heng Wu, Beisha Tang, Jifeng Guo
    Translational Neurodegeneration.2024;[Epub]     CrossRef
  • Microglia: roles and genetic risk in Parkinson’s disease
    Alex R. Trainor, Debra S. MacDonald, Jay Penney
    Frontiers in Neuroscience.2024;[Epub]     CrossRef
Viewpoint
Article image
Potential Benefits and Perils of Incorporating ChatGPT to the Movement Disorders Clinic
Andres Deik
J Mov Disord. 2023;16(2):158-162.   Published online May 24, 2023
DOI: https://doi.org/10.14802/jmd.23072
  • 3,642 View
  • 110 Download
  • 9 Web of Science
  • 8 Crossref
PDF

Citations

Citations to this article as recorded by  
  • Patient-Friendly Discharge Summaries in Korea Based on ChatGPT: Software Development and Validation
    Hanjae Kim, Hee Min Jin, Yoon Bin Jung, Seng Chan You
    Journal of Korean Medical Science.2024;[Epub]     CrossRef
  • A Survey of Clinicians' Views of the Utility of Large Language Models
    Matthew Spotnitz, Betina Idnay, Emily R. Gordon, Rebecca Shyu, Gongbo Zhang, Cong Liu, James J. Cimino, Chunhua Weng
    Applied Clinical Informatics.2024; 15(02): 306.     CrossRef
  • Performance of ChatGPT 3.5 and 4 as a tool for patient support before and after DBS surgery for Parkinson’s disease
    Ana Lúcia Oliveira, Miguel Coelho, Leonor Correia Guedes, Maria Begoña Cattoni, Herculano Carvalho, Pedro Duarte-Batista
    Neurological Sciences.2024; 45(12): 5757.     CrossRef
  • Artificial Intelligence in Medical Education and Mentoring in Rehabilitation Medicine
    Julie K. Silver, Mustafa Reha Dodurgali, Nara Gavini
    American Journal of Physical Medicine & Rehabilitation.2024; 103(11): 1039.     CrossRef
  • ChatGPT utilization within the building blocks of the healthcare services: A mixed-methods study
    Payam Shojaei, Mohsen Khosravi, Yalda Jafari, Amir Hossein Mahmoudi, Hadis Hassanipourmahani
    DIGITAL HEALTH.2024;[Epub]     CrossRef
  • Can ChatGPT diagnose my collapsing dog?
    Samira Abani, Steven De Decker, Andrea Tipold, Jasmin Nicole Nessler, Holger Andreas Volk
    Frontiers in Veterinary Science.2023;[Epub]     CrossRef
  • Bias and Inaccuracy in AI Chatbot Ophthalmologist Recommendations
    Michael C Oca, Leo Meller, Katherine Wilson, Alomi O Parikh, Allison McCoy, Jessica Chang, Rasika Sudharshan, Shreya Gupta, Sandy Zhang-Nunes
    Cureus.2023;[Epub]     CrossRef
  • (How) ChatGPT - Artificial Intelligence Thinks It Can Help/Harm Physiatry
    Jakub Jačisko, Viktor Veselý, Ke-Vin Chang, Levent Özçakar
    American Journal of Physical Medicine & Rehabilitation.2023;[Epub]     CrossRef
Review Article
Article image
Multiple System Atrophy: Advances in Diagnosis and Therapy
Hirohisa Watanabe, Sayuri Shima, Yasuaki Mizutani, Akihiro Ueda, Mizuki Ito
J Mov Disord. 2023;16(1):13-21.   Published online December 20, 2022
DOI: https://doi.org/10.14802/jmd.22082
  • 8,658 View
  • 576 Download
  • 7 Web of Science
  • 8 Crossref
AbstractAbstract PDF
This review summarizes improvements in understanding the pathophysiology and early clinical symptoms of multiple system atrophy (MSA) and advancements in diagnostic methods and disease-modifying therapies for the condition. In 2022, the Movement Disorder Society proposed new diagnostic criteria to develop disease-modifying therapies and promote clinical trials of MSA since the second consensus was proposed in 2008. Regarding pathogenesis, cutting-edge findings have accumulated on the interactions of α-synuclein, neuroinflammation, and oligodendroglia with neurons. In neuroimaging, introducing artificial intelligence, machine learning, and deep learning has notably improved diagnostic accuracy and individual analyses. Advancements in treatment have also been achieved, including immunotherapy therapy against α-synuclein and serotonin-targeted and mesenchymal stem cell therapies, which are thought to affect several aspects of the disease, including neuroinflammation. The accelerated progress in clarifying the pathogenesis of MSA over the past few years and the development of diagnostic techniques for detecting early-stage MSA are expected to facilitate the development of disease-modifying therapies for one of the most intractable neurodegenerative diseases.

Citations

Citations to this article as recorded by  
  • Integrative Analysis of Metabolome and Proteome in the Cerebrospinal Fluid of Patients with Multiple System Atrophy
    Nimisha Pradeep George, Minjun Kwon, Yong Eun Jang, Seok Gi Kim, Ji Su Hwang, Sang Seop Lee, Gwang Lee
    Cells.2025; 14(4): 265.     CrossRef
  • Characteristics of cerebral glucose metabolism in patients with cognitive impairment in multiple system atrophy
    Bin Chen, Lingchao Li, Lin Bai, Min Zhao, Ying Chang, Shi Gao
    Frontiers in Aging Neuroscience.2025;[Epub]     CrossRef
  • Comparing a BCI communication system in a patient with Multiple System Atrophy, with an animal model
    Brian Premchand, Kyaw Kyar Toe, Chuanchu Wang, Kai Rui Wan, Thevapriya Selvaratnam, Valerie Ethans Toh, Wai Hoe Ng, Camilo Libedinsky, Weiguo Chen, Ruiqi Lim, Ming-Yuan Cheng, Yuan Gao, Kai Keng Ang, Rosa Qi Yue So
    Brain Research Bulletin.2025; 223: 111289.     CrossRef
  • A Blinded Evaluation of Brain Morphometry for Differential Diagnosis of Atypical Parkinsonism
    Kazuya Kawabata, Florian Krismer, Beatrice Heim, Anna Hussl, Christoph Mueller, Christoph Scherfler, Elke R. Gizewski, Klaus Seppi, Werner Poewe
    Movement Disorders Clinical Practice.2024; 11(4): 381.     CrossRef
  • The potential of phosphorylated α‐synuclein as a biomarker for the diagnosis and monitoring of multiple system atrophy
    Toufik Abdul‐Rahman, Ranferi Eduardo Herrera‐Calderón, Arjun Ahluwalia, Andrew Awuah Wireko, Tomas Ferreira, Joecelyn Kirani Tan, Maximillian Wolfson, Shankhaneel Ghosh, Viktoriia Horbas, Vandana Garg, Asma Perveen, Marios Papadakis, Ghulam Md Ashraf, Ath
    CNS Neuroscience & Therapeutics.2024;[Epub]     CrossRef
  • Delivering the diagnosis of multiple system atrophy: a multicenter survey on Japanese neurologists’ perspectives
    Miki Yoshitake, Atsuhiko Sugiyama, Takayoshi Shimohata, Nobuyuki Araki, Masahide Suzuki, Kazumoto Shibuya, Kengo Nagashima, Nobutaka Hattori, Satoshi Kuwabara
    BMC Neurology.2024;[Epub]     CrossRef
  • Clinical comparison of the 2008 and 2022 diagnostic criteria for early multiple system atrophy-cerebellar type
    Seoyeon Kim, Kyung Ah Woo, Jung Hwan Shin, Han-Joon Kim, Beomseok Jeon
    Clinical Autonomic Research.2024; 34(6): 609.     CrossRef
  • Ocular Vestibular-Evoked Myogenic Potential Assists in the Differentiation of Multiple System Atrophy From Parkinson’s Disease
    Keun-Tae Kim, Kyoungwon Baik, Sun-Uk Lee, Euyhyun Park, Chan-Nyoung Lee, Tonghoon Woo, Yukang Kim, Seoui Kwag, Hyunsoh Park, Ji-Soo Kim
    Journal of Movement Disorders.2024; 17(4): 398.     CrossRef
Original Article
Article image
The Effect of Blood Lipids, Type 2 Diabetes, and Body Mass Index on Parkinson’s Disease: A Korean Mendelian Randomization Study
Kye Won Park, Yun Su Hwang, Seung Hyun Lee, Sungyang Jo, Sun Ju Chung
J Mov Disord. 2023;16(1):79-85.   Published online January 12, 2023
DOI: https://doi.org/10.14802/jmd.22175
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AbstractAbstract PDFSupplementary Material
Objective
Associations between various metabolic conditions and Parkinson’s disease (PD) have been previously identified in epidemiological studies. We aimed to investigate the causal effect of lipid levels, type 2 diabetes mellitus (T2DM), and body mass index (BMI) on PD in a Korean population via Mendelian randomization (MR).
Methods
Two-sample MR analyses were performed with inverse-variance weighted (IVW), weighted median, and MR-Egger regression approaches. We identified genetic variants associated with lipid concentrations, T2DM, and BMI in publicly available summary statistics, which were either collected from genome-wide association studies (GWASs) or from meta-analyses of GWAS that targeted only Korean individuals or East Asian individuals, including Korean individuals. The outcome dataset was a GWAS on PD performed in a Korean population.
Results
From previous GWASs and meta-analyses, we selected single nucleotide polymorphisms as the instrumental variables. Variants associated with serum levels of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides, as well as with T2DM and BMI, were selected (n = 11, 19, 17, 89, and 9, respectively). There were no statistically significant causal associations observed between the five exposures and PD using either the IVW, weighted median, or MR-Egger methods (p-values of the IVW method: 0.332, 0.610, 0.634, 0.275, and 0.860, respectively).
Conclusion
This study does not support a clinically relevant causal effect of lipid levels, T2DM, and BMI on PD risk in a Korean population.

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  • Genetic evidence for the liver-brain axis: lipid metabolism and neurodegenerative disease risk
    Zeyu Wang, Zixiao Yin, Guangyong Sun, Dong Zhang, Jianguo Zhang
    Lipids in Health and Disease.2025;[Epub]     CrossRef
  • Causal effect of systemic lupus erythematosus on psychiatric disorders: A two-sample Mendelian randomization study
    Hua Xue, Shuangjuan Liu, Li Zeng, Wenhui Fan
    Journal of Affective Disorders.2024; 347: 422.     CrossRef
  • Causal relationship between diabetes mellitus, glycemic traits and Parkinson’s disease: a multivariable mendelian randomization analysis
    Qitong Wang, Benchi Cai, Lifan Zhong, Jitrawadee Intirach, Tao Chen
    Diabetology & Metabolic Syndrome.2024;[Epub]     CrossRef
  • Association of Body Mass Index and Parkinson Disease
    Cloé Domenighetti, Pierre-Emmanuel Sugier, Ashwin Ashok Kumar Sreelatha, Claudia Schulte, Sandeep Grover, Berta Portugal, Pei-Chen Lee, Patrick May, Dheeraj Bobbili, Milena Radivojkov Blagojevic, Peter Lichtner, Andrew B. Singleton, Dena Hernandez, Connor
    Neurology.2024;[Epub]     CrossRef
  • Causal association between common rheumatic diseases and arrhythmia: a Mendelian randomization study
    Yuchen Zhang, Ling Tang, Ke Zhang, Xinai Meng, Tian Liu, Yanjia Chen, Xingfu Huang
    Frontiers in Cardiovascular Medicine.2024;[Epub]     CrossRef
  • Unraveling the link: exploring the causal relationship between diabetes, multiple sclerosis, migraine, and Alzheimer’s disease through Mendelian randomization
    Hua Xue, Li Zeng, Shuangjuan Liu
    Frontiers in Neuroscience.2023;[Epub]     CrossRef
  • Glycated hemoglobin A1c, cerebral small vessel disease burden, and disease severity in Parkinson's disease
    Xinxin Ma, Shuhua Li, Fengzhi Liu, Yu Du, Haibo Chen, Wen Su
    Annals of Clinical and Translational Neurology.2023; 10(12): 2276.     CrossRef
Review Articles
Article image
α-Synuclein: A Promising Biomarker for Parkinson’s Disease and Related Disorders
Taku Hatano, Ayami Okuzumi, Gen Matsumoto, Taiji Tsunemi, Nobutaka Hattori
J Mov Disord. 2024;17(2):127-137.   Published online April 9, 2024
DOI: https://doi.org/10.14802/jmd.24075
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AbstractAbstract PDF
Mutations in the SNCA gene, which encodes α-synuclein (α-syn), play a key role in the development of genetic Parkinson’s disease (PD). α-Syn is a major component of Lewy bodies in PD and glial cytoplasmic inclusions in multiple system atrophy (MSA). Rapid eye movement sleep behavior disorder patients often progress to PD, dementia with Lewy bodies, or MSA, which are collectively known as α-synucleinopathies. The loss of dopaminergic neurons with Lewy bodies precedes motor dysfunction in these diseases, but the mechanisms of neurodegeneration due to α-syn aggregation are poorly understood. Monitoring α-syn aggregation in vivo could serve as a diagnostic biomarker and help elucidate pathogenesis, necessitating a simple and accurate detection method. Seed amplification assays (SAAs), such as real-time quaking-induced conversion and protein misfolding cyclic amplification, are used to detect small amounts of abnormally structured α-syn protofibrils, which are central to aggregation. These methods are promising for the early diagnosis of α-synucleinopathy. Differences in α-syn filament structures between α-synucleinopathies, as observed through transmission electron microscopy and cryo-electron microscopy, suggest their role in the pathogenesis of neurodegeneration. SAAs may differentiate between subtypes of α-synucleinopathy and other diseases. Efforts are also being made to identify α-syn from blood using various methods. This review introduces body fluid α-syn biomarkers based on pathogenic α-syn seeds, which are expected to redefine α-synucleinopathy diagnosis and staging, improving clinical research accuracy and facilitating biomarker development.

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  • Selective detection of alpha synuclein amyloid fibrils by faradaic and non-faradaic electrochemical impedance spectroscopic approaches
    Hussaini Adam, Subash C.B. Gopinath, Hemavathi Krishnan, Tijjani Adam, Makram A. Fakhri, Evan T. Salim, A. Shamsher, Sreeramanan Subramaniam, Yeng Chen
    Bioelectrochemistry.2025; 161: 108800.     CrossRef
  • Evolving Landscape of Parkinson’s Disease Research: Challenges and Perspectives
    Rumiana Tenchov, Janet M. Sasso, Qiongqiong Angela Zhou
    ACS Omega.2025; 10(2): 1864.     CrossRef
  • Seeding amplification assay: Limitations and insights for enhanced clinical and research applications
    Ilham Y Abdi, Sara A Hashish, Omar A El-Agnaf
    Journal of Parkinson’s Disease.2025;[Epub]     CrossRef
  • Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets
    Yuanyuan Gao, Jiarui Zhang, Tuoxian Tang, Zhenjiang Liu
    International Journal of Molecular Sciences.2024; 25(19): 10484.     CrossRef
  • Circadian rhythm disruption: a potential trigger in Parkinson’s disease pathogenesis
    Ke Xu, Yu Zhang, Yue Shi, Yake Zhang, Chengguang Zhang, Tianjiao Wang, Peizhu Lv, Yan Bai, Shun Wang
    Frontiers in Cellular Neuroscience.2024;[Epub]     CrossRef
A Brief History of NBIA Gene Discovery
Susan J. Hayflick
J Mov Disord. 2023;16(2):133-137.   Published online April 26, 2023
DOI: https://doi.org/10.14802/jmd.23014
  • 3,531 View
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AbstractAbstract PDF
Neurodegenerative disorders associated with high basal ganglia iron are known by the overarching term of ‘NBIA’ disorders or ‘neurodegeneration with brain iron accumulation’. Discovery of their individual genetic bases was greatly enabled by the collection of DNA and clinical data in just a few centers. With each discovery, the remaining idiopathic disorders could be further stratified by common clinical, radiographic or pathological features to enable the next hunt. This iterative process, along with strong and open collaborations, enabled the discoveries of PANK2, PLA2G6, C19orf12, FA2H, WDR45, and COASY gene mutations as underlying PKAN, PLAN, MPAN, FAHN, BPAN, and CoPAN, respectively. The era of Mendelian disease gene discovery is largely behind us, but the history of these discoveries for the NBIA disorders has not yet been told. A brief history is offered here.

Citations

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  • Metabolic impairments in neurodegeneration with brain iron accumulation
    Agata Wydrych, Barbara Pakuła, Justyna Janikiewicz, Aneta M. Dobosz, Patrycja Jakubek-Olszewska, Marta Skowrońska, Iwona Kurkowska-Jastrzębska, Maciej Cwyl, Mariola Popielarz, Paolo Pinton, Barbara Zavan, Agnieszka Dobrzyń, Magdalena Lebiedzińska-Arciszew
    Biochimica et Biophysica Acta (BBA) - Bioenergetics.2025; 1866(1): 149517.     CrossRef
  • Iron metabolism and ferroptosis in health and diseases: the crucial role of mitochondria in meta-bolically active tissues
    Angela Catapano, Fabiano Cimmino, Lidia Petrella, Amelia Pizzella, Margherita D'Angelo, Katia Ambrosio, Francesca Marino, Annarita Sabbatini, Massimiliano Petrelli, Barbara Paolini, Lucio Lucchin, Gina Cavaliere, Luigia Cristino, Marianna Crispino, Giovan
    The Journal of Nutritional Biochemistry.2025; : 109888.     CrossRef
  • Mitochondrial iron deficiency triggers cytosolic iron overload in PKAN hiPS-derived astrocytes
    Paolo Santambrogio, Anna Cozzi, Chiara Balestrucci, Maddalena Ripamonti, Valeria Berno, Eugenia Cammarota, Andrea Stefano Moro, Sonia Levi
    Cell Death & Disease.2024;[Epub]     CrossRef
  • Iron Dyshomeostasis in Neurodegeneration with Brain Iron Accumulation (NBIA): Is It the Cause or the Effect?
    Francesco Agostini, Bibiana Sgalletta, Marco Bisaglia
    Cells.2024; 13(16): 1376.     CrossRef
  • COASY Protein-Associated Neurodegeneration: Report from India
    Rohan R. Mahale, Raviprakash Singh, Pavankumar Katragadda, Hansashree Padmanabha
    Annals of Indian Academy of Neurology.2023; 26(5): 834.     CrossRef
Original Article
Article image
High Levels of Mutant Huntingtin Protein in Tear Fluid From Huntington’s Disease Gene Expansion Carriers
Marlies Gijs, Nynke Jorna, Nicole Datson, Chantal Beekman, Cira Dansokho, Alexander Weiss, David E. J. Linden, Mayke Oosterloo
J Mov Disord. 2024;17(2):181-188.   Published online February 21, 2024
DOI: https://doi.org/10.14802/jmd.24014
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AbstractAbstract PDFSupplementary Material
Objective
Huntington’s disease (HD) is an autosomal dominant, fully penetrant, neurodegenerative disease that most commonly affects middle-aged adults. HD is caused by a CAG repeat expansion in the HTT gene, resulting in the expression of mutant huntingtin (mHTT). Our aim was to detect and quantify mHTT in tear fluid, which, to our knowledge, has never been measured before.
Methods
We recruited 20 manifest and 13 premanifest HD gene expansion carriers, and 20 age-matched controls. All patients underwent detailed assessments, including the Unified Huntington’s Disease Rating Scale (UHDRS) total motor score (TMS) and total functional capacity (TFC) score. Tear fluid was collected using paper Schirmer’s strips. The level of tear mHTT was determined using single-molecule counting SMCxPRO technology.
Results
The average tear mHTT levels in manifest (67,223 ± 80,360 fM) and premanifest patients (55,561 ± 45,931 fM) were significantly higher than those in controls (1,622 ± 2,179 fM). We noted significant correlations between tear mHTT levels and CAG repeat length, “estimated years to diagnosis,” disease burden score and UHDRS TMS and TFC. The receiver operating curve demonstrated an almost perfect score (area under the curve [AUC] = 0.9975) when comparing controls to manifest patients. Similarly, the AUC between controls and premanifest patients was 0.9846. The optimal cutoff value for distinguishing between controls and manifest patients was 4,544 fM, whereas it was 6,596 fM for distinguishing between controls and premanifest patients.
Conclusion
Tear mHTT has potential for early and noninvasive detection of alterations in HD patients and could be integrated into both clinical trials and clinical diagnostics.

Citations

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  • A comprehensive scoping review of methodological approaches and clinical applications of tear fluid biomarkers
    Marlies Gijs, Nienke van de Sande, Clémence Bonnet, Jente Schmeetz, Rosa Fernandes, Sònia Travé-Huarte, Marcela Huertas-Bello, Jeremy Chung Bo Chiang, Nikolay Boychev, Shruti Sharma, Françoise Brignole-Baudouin, Karima Kessal, Paul Lingor, Maurice M.T.H.
    Progress in Retinal and Eye Research.2025; 106: 101338.     CrossRef
  • Global practices of tear fluid collection, storage, and molecular analysis – A questionnaire by the Tear Research Network
    Nikolay Boychev, Swaminathan Sethu, Romy Op de Laak, Marlies Gijs
    Contact Lens and Anterior Eye.2025; : 102388.     CrossRef
  • Unveiling brain disorders using liquid biopsy and Raman spectroscopy
    Jeewan C. Ranasinghe, Ziyang Wang, Shengxi Huang
    Nanoscale.2024; 16(25): 11879.     CrossRef
  • Ocular tear fluid biomarkers collected by contact lenses
    Nikolay Boychev, Vincent Yeung, Menglu Yang, Levi N. Kanu, Amy E. Ross, Liangju Kuang, Lin Chen, Joseph B. Ciolino
    Biochemical and Biophysical Research Communications.2024; 734: 150744.     CrossRef
Review Article
Article image
Ultrastructures of α-Synuclein Filaments in Synucleinopathy Brains and Experimental Models
Airi Tarutani, Masato Hasegawa
J Mov Disord. 2024;17(1):15-29.   Published online November 22, 2023
DOI: https://doi.org/10.14802/jmd.23213
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AbstractAbstract PDF
Intracellular α-synuclein (α-syn) inclusions are a neuropathological hallmark of Lewy body disease (LBD) and multiple system atrophy (MSA), both of which are termed synucleinopathies. LBD is defined by Lewy bodies and Lewy neurites in neurons, while MSA displays glial cytoplasmic inclusions in oligodendrocytes. Pathological α-syn adopts an ordered filamentous structure with a 5–10 nm filament diameter, and this conformational change has been suggested to be involved in the disease onset and progression. Synucleinopathies also exhibit characteristic ultrastructural and biochemical properties of α-syn filaments, and α-syn strains with distinct conformations have been identified. Numerous experimental studies have supported the idea that pathological α-syn self-amplifies and spreads throughout the brain, during which processes the conformation of α-syn filaments may drive the disease specificity. In this review, we summarize the ultrastructural features and heterogeneity of α-syn filaments in the brains of patients with synucleinopathy and in experimental models of seeded α-syn aggregation.

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  • Positron emission tomography tracers for synucleinopathies
    Jie Xiang, Zhentao Zhang, Shengxi Wu, Keqiang Ye
    Molecular Neurodegeneration.2025;[Epub]     CrossRef
  • Correlative light and electron microscopy imaging of proteinaceous deposits in cell cultures and brain tissues
    Peizhou Jiang, Dennis W. Dickson
    Acta Neuropathologica Communications.2025;[Epub]     CrossRef
  • α-Synuclein: A Promising Biomarker for Parkinson’s Disease and Related Disorders
    Taku Hatano, Ayami Okuzumi, Gen Matsumoto, Taiji Tsunemi, Nobutaka Hattori
    Journal of Movement Disorders.2024; 17(2): 127.     CrossRef
  • Exploring the Potential of Biomimetic Peptides in Targeting Fibrillar and Filamentous Alpha-Synuclein—An In Silico and Experimental Approach to Parkinson’s Disease
    Sophia A. Frantzeskos, Mary A. Biggs, Ipsita A. Banerjee
    Biomimetics.2024; 9(11): 705.     CrossRef
Original Article
Article image
Caregiver Burden of Patients With Huntington’s Disease in South Korea
Chan Young Lee, Chaewon Shin, Yun Su Hwang, Eungseok Oh, Manho Kim, Hyun Sook Kim, Sun Ju Chung, Young Hee Sung, Won Tae Yoon, Jin Whan Cho, Jae-Hyeok Lee, Han-Joon Kim, Hee Jin Chang, Beomseok Jeon, Kyung Ah Woo, Seong-Beom Koh, Kyum-Yil Kwon, Jangsup Moon, Young Eun Kim, Jee-Young Lee
J Mov Disord. 2024;17(1):30-37.   Published online September 11, 2023
DOI: https://doi.org/10.14802/jmd.23134
  • 4,712 View
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  • 1 Comments
AbstractAbstract PDFSupplementary Material
Objective
This is the first prospective cohort study of Huntington’s disease (HD) in Korea. This study aimed to investigate the caregiver burden in relation to the characteristics of patients and caregivers.
Methods
From August 2020 to February 2022, we enrolled patients with HD from 13 university hospitals in Korea. We used the 12-item Zarit Burden Interview (ZBI-12) to evaluate the caregiver burden. We evaluated the clinical associations of the ZBI-12 scores by linear regression analysis and investigated the differences between the low- and high-burden groups.
Results
Sixty-five patients with HD and 45 caregivers were enrolled in this cohort study. The average age at onset of motor symptoms was 49.3 ± 12.3 years, with an average cytosine-adenine-guanine (CAG)n of 42.9 ± 4.0 (38–65). The median ZBI-12 score among our caregivers was 17.6 ± 14.2. A higher caregiver burden was associated with a more severe Shoulson–Fahn stage (p = 0.038) of the patients. A higher ZBI-12 score was also associated with lower independence scale (B = -0.154, p = 0.006) and functional capacity (B = -1.082, p = 0.002) scores of patients. The caregiving duration was longer in the high- than in the low-burden group. Caregivers’ demographics, blood relation, and marital and social status did not affect the burden significantly.
Conclusion
HD patients’ neurological status exerts an enormous impact on the caregiver burden regardless of the demographic or social status of the caregiver. This study emphasizes the need to establish an optimal support system for families dealing with HD in Korea. A future longitudinal analysis could help us understand how disease progression aggravates the caregiver burden throughout the entire disease course.

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  • Non-Pharmacological Interventions for Caregivers of People with Motor Neurone Disease: A Scoping Review of Psychosocial Outcomes
    Chidera Okoh, Leighanne Mayall, Selina M. Makin, Cliff Chen, Nicolò Zarotti
    Brain Sciences.2025; 15(2): 112.     CrossRef
  • A Practical Guide for Diagnostic Investigations and Special Considerations in Patients With Huntington’s Disease in Korea
    Jangsup Moon, Eungseok Oh, Minkyeong Kim, Ryul Kim, Dallah Yoo, Chaewon Shin, Jee-Young Lee, Jong-Min Kim, Seong-Beom Koh, Manho Kim, Beomseok Jeon
    Journal of Movement Disorders.2025; 18(1): 17.     CrossRef
  • A Practical Guide for Clinical Approach to Patients With Huntington’s Disease in Korea
    Chaewon Shin, Ryul Kim, Dallah Yoo, Eungseok Oh, Jangsup Moon, Minkyeong Kim, Jee-Young Lee, Jong-Min Kim, Seong-Beom Koh, Manho Kim, Beomseok Jeon
    Journal of Movement Disorders.2024; 17(2): 138.     CrossRef
  • Attitude toward physical activity among Asian American family caregivers of persons living with dementia
    JiWon Choi, Van Park, Andrew Jung, Janice Tsoh
    Geriatric Nursing.2024;[Epub]     CrossRef
Viewpoint
Article image
From Evidence to the Dish: A Viewpoint of Implementing a Thai-Style Mediterranean Diet for Parkinson’s Disease
Onanong Phokaewvarangkul, Nitinan Kantachadvanich, Vijittra Buranasrikul, Appasone Phoumindr, Saisamorn Phumphid, Priya Jagota, Roongroj Bhidayasiri
J Mov Disord. 2023;16(3):279-284.   Published online June 19, 2023
DOI: https://doi.org/10.14802/jmd.23021
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PDFSupplementary Material

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  • The centenarian blueprint: lessons in defying Parkinson’s disease
    Roongroj Bhidayasiri, Ikuko Aiba, Masahiro Nomoto
    Journal of Neural Transmission.2025; 132(3): 331.     CrossRef
  • Old problems, new solutions: harnessing technology and innovation in Parkinson’s disease—evidence and experiences from Thailand
    Roongroj Bhidayasiri
    Journal of Neural Transmission.2024; 131(6): 721.     CrossRef
  • The rise of Parkinson’s disease is a global challenge, but efforts to tackle this must begin at a national level: a protocol for national digital screening and “eat, move, sleep” lifestyle interventions to prevent or slow the rise of non-communicable dise
    Roongroj Bhidayasiri, Jirada Sringean, Saisamorn Phumphid, Chanawat Anan, Chusak Thanawattano, Suwijak Deoisres, Pattamon Panyakaew, Onanong Phokaewvarangkul, Suppata Maytharakcheep, Vijittra Buranasrikul, Tittaya Prasertpan, Rotjana Khontong, Priya Jagot
    Frontiers in Neurology.2024;[Epub]     CrossRef
  • Personalized nutrition: the end of the one-diet-fits-all era
    Sonia Roman, Liliana Campos-Medina, Leonardo Leal-Mercado
    Frontiers in Nutrition.2024;[Epub]     CrossRef
Brief communication
Sex and Gender Influence Urinary Symptoms and Management in Multiple System Atrophy
Elke Schipani Bailey, Sara J. Hooshmand, Negin Badihian, Paola Sandroni, Eduardo E. Benarroch, James H. Bower, Phillip A. Low, Wolfgang Singer, Elizabeth A. Coon
J Mov Disord. 2023;16(2):196-201.   Published online May 24, 2023
DOI: https://doi.org/10.14802/jmd.23016
  • 3,076 View
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AbstractAbstract PDF
Objective
Multiple system atrophy (MSA) is characterized by urinary dysfunction, yet the influence of sex and gender on urinary symptoms and treatment is unclear. We sought to characterize sex and gender differences in the symptomatology, evaluation, and management of urinary dysfunction in patients with MSA.
Methods
Patients with MSA evaluated at our institution were reviewed and stratified by sex.
Results
While the prevalence of urinary symptoms was similar in male and female patients, incontinence was more common in females. Despite this, males and females underwent postvoid residual (PVR) measurement at similar rates. While catheterization rates were similar when PVR was measured, males were more than twice as likely to be catheterized than females in the absence of PVR measurement.
Conclusion
Urinary symptoms are common in MSA, but their presentation differs between males and females. The difference in catheterization rates may be driven by a gender disparity in referrals for PVR, which can guide treatment.

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  • Multiple system atrophy related neurogenic bladder: mechanism and treatment
    Gengqing Ren, Yao Wang, Hao Tian, Kaige Zhang, Han Zhang, Xiaoxu Liu, Zhigang Chen
    Neurological Sciences.2025;[Epub]     CrossRef
  • In vivo cerebral metabolic and dopaminergic characteristics in multiple system atrophy with orthostatic hypotension
    Chenxi Xue, Xiaofeng Dou, Congcong Yu, Yan Zhong, Jing Wang, Xiang Zhang, Le Xue, Daoyan Hu, Shuang Wu, Hong Zhang, Mei Tian
    European Journal of Nuclear Medicine and Molecular Imaging.2024; 51(2): 468.     CrossRef
  • Sex-related differences in the clinical presentation of multiple system atrophy
    Fabian Leys, Sabine Eschlböck, Nicole Campese, Philipp Mahlknecht, Marina Peball, Georg Goebel, Victoria Sidoroff, Florian Krismer, Roberta Granata, Stefan Kiechl, Werner Poewe, Klaus Seppi, Gregor K. Wenning, Alessandra Fanciulli
    Clinical Autonomic Research.2024; 34(2): 253.     CrossRef
  • Revisiting sex-gender disparities in MSA: An unfinished narrative
    Alexandra Pérez-Soriano, Celia Painous, Barbara Segura, Maria José Martí
    Parkinsonism & Related Disorders.2024; 129: 107159.     CrossRef
Original Article
Article image
The Clinical Characterization of Blocking Tics in Patients With Tourette Syndrome
José Fidel Baizabal-Carvallo, Joseph Jankovic
J Mov Disord. 2023;16(2):163-167.   Published online March 7, 2023
DOI: https://doi.org/10.14802/jmd.22122
  • 4,130 View
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AbstractAbstract PDFSupplementary Material
Objective
Tourette syndrome (TS) is a neurodevelopmental disorder characterized by the presence of motor and phonic tics. Blocking phenomena, characterized by arrests in motor activity causing interruptions in movements or speech, have also been described in patients with TS. In this study, we aimed to characterize the frequency and features of blocking tics in patients with TS.
Methods
We studied a cohort of 201 patients with TS evaluated at our movement disorders clinic.
Results
We identified 12 (6%) patients with blocking phenomena. Phonic tic intrusion causing speech arrest was the most common (n = 8, 4%), followed by sustained isometric muscle contractions arresting body movements (n = 4, 2%). The following variables were statistically related to blocking phenomena: shoulder tics, leg tics, copropraxia, dystonic tics, simple phonic tics, and number of phonic tics per patient (all p < 0.050). In the multivariate regression, the presence of dystonic tics (p = 0.014) and a higher number of phonic tics (p = 0.022) were associated with blocking phenomena.
Conclusion
Blocking phenomena are present in approximately 6% of patients with TS, and the presence of dystonic tics and a higher frequency and number of phonic tics increase the risk for these phenomena.

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  • Tics emergencies and malignant tourette syndrome: Assessment and management
    José Fidel Baizabal-Carvallo, Andrea E. Cavanna, Joseph Jankovic
    Neuroscience & Biobehavioral Reviews.2024; 159: 105609.     CrossRef
  • Tourette syndrome research highlights from 2023
    Andreas Hartmann, Per Andrén, Cyril Atkinson-Clement, Virginie Czernecki, Cécile Delorme, Nanette Mol Debes, Simon Morand-Beaulieu, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Kevin J. Black
    F1000Research.2024; 13: 677.     CrossRef
  • Tourette syndrome research highlights from 2023
    Andreas Hartmann, Per Andrén, Cyril Atkinson-Clement, Virginie Czernecki, Cécile Delorme, Nanette Mol Debes, Simon Morand-Beaulieu, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Kevin J. Black
    F1000Research.2024; 13: 677.     CrossRef
  • Oromandibular tics associated with Tourette syndrome
    José Fidel Baizabal-Carvallo, Marlene Alonso-Juarez, Joseph Jankovic
    Journal of Neurology.2023; 270(5): 2591.     CrossRef

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