Journal of Movement Disorders

Most-read articles are from the articles published in 2022 during the last three month.

Review Articles

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

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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

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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
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

Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease: Yen-Chung Chen, Wei-Sheng Wang, Simon J G Lewis, Shey-Lin Wu; J Mov Disord. 2024;17(1):1-14. Published online November 21, 2023; DOI: https://doi.org/10.14802/jmd.23216

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Abstract PDF: Circadian disruption is being increasingly recognized as a critical factor in the development and progression of Parkinson’s disease (PD). This review aims to provide an in-depth overview of the relationship between circadian disruption and PD by exploring the molecular, cellular, and behavioral aspects of this interaction. This review will include a comprehensive understanding of how the clock gene system and transcription–translation feedback loops function and how they are diminished in PD. The article also discusses the role of clock genes in the regulation of circadian rhythms, as well as the impact of clock gene dysregulation on mitochondrial function, oxidative stress, and neuroinflammation, including the microbiota-gut-brain axis, which have all been proposed as being crucial mechanisms in the pathophysiology of PD. Finally, this review highlights potential therapeutic strategies targeting the clock gene system and circadian rhythm for the treatment of PD.

Original Article

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

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Abstract PDF Supplementary 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.

Review Articles

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

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Abstract 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

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;[Epub] CrossRef

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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Abstract 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.

Original Article

Umami and Other Taste Perceptions in Patients With Parkinson’s Disease: Priya Jagota, Nattida Chotechuang, Chanawat Anan, Teeraparp Kitjawijit, Chanchai Boonla, Roongroj Bhidayasiri; J Mov Disord. 2022;15(2):115-123. Published online March 22, 2022; DOI: https://doi.org/10.14802/jmd.21058

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Abstract PDF

Objective
Studies of taste perceptions in Parkinson’s disease (PD) patients have been controversial, and none of these studies have assessed umami taste. This study aimed to assess umami, along with the other 4 taste functions in PD patients.
Methods
Participants were tested for gustation using the modified filter paper disc method and olfaction using the modified Sniffin’ Stick-16 (mSS-16) test (only 14 culturally suitable items were used). A questionnaire evaluated patients’ subjective olfactory and gustatory dysfunction, taste preference, appetite, and food habits.
Results
A total of 105 PD patients and 101 age- and sex-matched controls were included. The body mass index (BMI) of PD patients was lower than that of controls (PD = 22.62, controls = 23.86, p = 0.028). The mSS-16 score was 10.7 for controls and 6.4 for PD patients (p < 0.001) (normal ≥ 9). Taste recognition thresholds (RTs) for sweet, salty, sour, bitter and umami tastes were significantly higher in PD, indicating poorer gustation. All taste RTs correlated with each other, except for umami. Most patients were unaware of their dysfunction. Patients preferred sweet, salty and umami tastes more than the controls. Dysgeusia of different tastes in patients was differentially associated with poorer discrimination of tastes, an inability to identify the dish and adding extra seasoning to food. BMI and mSS-16 scores showed no correlation in either patients or controls.
Conclusion
PD patients have dysgeusia for all five tastes, including umami, which affects their appetite and diet. Patients preferred sweet, salty and umami tastes. This information can help adjust patients’ diets to improve their nutritional status.

Citations

Citations to this article as recorded by

The missing piece of the puzzle – The key role of the dietitian in the management of Parkinson's disease
Richelle Flanagan, Carley Rusch, Fiona E. Lithander, Indu Subramanian
Parkinsonism & Related Disorders.2024; 121: 106021. CrossRef
Body mass index in patients with Parkinson’s disease: a systematic review
Yinghui Li, Yumei Liu, Chuanning Du, Jun Wang
Journal of Neurophysiology.2024; 131(2): 311. CrossRef
Apnea behavior in early- and late-stage mouse models of Parkinson's disease: Cineradiographic analysis of spontaneous breathing, acute stress, and swallowing
Lorena Roberta de Souza Mendes Kawamura, Max Sarmet, Priscila Sales de Campos, Sachiko Takehara, Yasuhiro Kumei, Jorge Luis Lopes Zeredo
Respiratory Physiology & Neurobiology.2024; 323: 104239. CrossRef
Gustatory dysfunction is related to Parkinson's disease: A systematic review and meta‐analysis
Il‐Youp Kwak, Kyung Soo Kim, Hyun Jin Min
International Forum of Allergy & Rhinology.2023; 13(10): 1949. CrossRef

Review Articles

Adult-Onset Genetic Leukoencephalopathies With Movement Disorders: Mu-Hui Fu, Yung-Yee Chang; J Mov Disord. 2023;16(2):115-132. Published online March 7, 2023; DOI: https://doi.org/10.14802/jmd.22127

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Abstract PDF: Genetic leukoencephalopathies (GLEs) are a group of white matter abnormalities with heterogeneous radiological and phenotypic features. Although these conditions have mostly been described in children, adult-onset cases are increasingly recognized owing to the widespread use of neuroimaging and advances in molecular genetic testing. The disease course is often progressive with a varied spectrum of presentations, trapping neurologists in the dilemma of differential diagnosis. Movement disorders are among the most common symptoms, and their diversity makes diagnosis challenging. In this review, we focus on adult-onset GLEs with movement disorders and offer a step-by-step diagnostic approach by clarifying the phenomenology of movement, advising investigations for acquired causes, describing the clinical and radiological clues to each disease, emphasizing the limitations of advanced molecular testing, and discussing the future application of artificial intelligence. We provide a list summarizing the leukoencephalopathies associated with different categories of movement disorders. In addition to guiding clinicians on how to narrow the list of differential diagnoses with the tools currently available, another aim of this review is to emphasize the inevitable trend toward applying advanced technology in diagnosing these difficult diseases.

Nine Hereditary Movement Disorders First Described in Asia: Their History and Evolution: Priya Jagota, Yoshikazu Ugawa, Zakiyah Aldaajani, Norlinah Mohamed Ibrahim, Hiroyuki Ishiura, Yoshiko Nomura, Shoji Tsuji, Cid Diesta, Nobutaka Hattori, Osamu Onodera, Saeed Bohlega, Amir Al-Din, Shen-Yang Lim, Jee-Young Lee, Beomseok Jeon, Pramod Kumar Pal, Huifang Shang, Shinsuke Fujioka, Prashanth Lingappa Kukkle, Onanong Phokaewvarangkul, Chin-Hsien Lin, Cholpon Shambetova, Roongroj Bhidayasiri; J Mov Disord. 2023;16(3):231-247. Published online June 13, 2023; DOI: https://doi.org/10.14802/jmd.23065

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Abstract PDF Supplementary Material: Clinical case studies and reporting are important to the discovery of new disorders and the advancement of medical sciences. Both clinicians and basic scientists play equally important roles leading to treatment discoveries for both cures and symptoms. In the field of movement disorders, exceptional observation of patients from clinicians is imperative, not just for phenomenology but also for the variable occurrences of these disorders, along with other signs and symptoms, throughout the day and the disease course. The Movement Disorders in Asia Task Force (TF) was formed to help enhance and promote collaboration and research on movement disorders within the region. As a start, the TF has reviewed the original studies of the movement disorders that were preliminarily described in the region. These include nine disorders that were first described in Asia: Segawa disease, PARK-Parkin, X-linked dystonia-parkinsonism, dentatorubral-pallidoluysian atrophy, Woodhouse-Sakati syndrome, benign adult familial myoclonic epilepsy, Kufor-Rakeb disease, tremulous dystonia associated with mutation of the calmodulin-binding transcription activator 2 gene, and paroxysmal kinesigenic dyskinesia. We hope that the information provided will honor the original researchers and help us learn and understand how earlier neurologists and basic scientists together discovered new disorders and made advances in the field, which impact us all to this day.

Original Articles

Premonitory Urges Reconsidered: Urge Location Corresponds to Tic Location in Patients With Primary Tic Disorders: Jana Essing, Ewgeni Jakubovski, Nikolas Psathakis, Sinan N Cevirme, James F Leckman, Kirsten R Müller-Vahl; J Mov Disord. 2022;15(1):43-52. Published online January 25, 2022; DOI: https://doi.org/10.14802/jmd.21045

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Abstract PDF Supplementary Material

Objective
In patients with Tourette syndrome and other primary tic disorders (PTDs), tics are typically preceded by premonitory urges (PUs). To date, only a few studies have investigated the location and frequency of PUs, and contrary to clinical experience, the results suggest that PUs are not located in the same anatomic region as the tics. This study aimed to further explore PU location and frequency in detail, differentiating the kind and complexity of the corresponding tics, in a large sample of patients with PTD.
Methods
A total of 291 adult (≥ 18 years) patients with a confirmed diagnosis of chronic PTD were included. The study was conducted online, assement included tics and the general characterization of PUs and a sophisticated body drawing for locating PUs.
Results
We found that PUs were located in the same body area as, or in direct proximity to, the corresponding tic. Most frequently, PUs were located in the face and at the head (62.1%). Compared with simple tics, complex (motor and vocal) tics were more often preceded by a PU; but there was no difference in PU frequency observed between motor tics and vocal tics. PUs were more often experienced at the front than at the back of the body (73% vs. 27%), while there was no difference between the right and left sides (41.6% vs. 41.3%).
Conclusion
The strong association between PU and tic location further supports the hypothesis that PUs represent the core of PTD. Accordingly, future therapies should focus on treating PUs to achieve greater tic reduction.

Citations

Citations to this article as recorded by

Functional Tic‐Like Behaviors: A Common Comorbidity in Patients with Tourette Syndrome
Kirsten R. Müller‐Vahl, Anna Pisarenko, Carolin Fremer, Martina Haas, Ewgeni Jakubovski, Natalia Szejko
Movement Disorders Clinical Practice.2024; 11(3): 227. CrossRef
Parent-Report Sleep Disturbances and Everyday Executive Functioning Difficulties in Children with Tourette Syndrome
Lisa Keenan, Jessica Bramham, Michelle Downes
Developmental Neuropsychology.2024; 49(1): 39. CrossRef
Premonitory Urge in Patients with Tics and Functional Tic‐like Behaviors
Natalia Szejko, Julian Fletcher, Davide Martino, Tamara Pringsheim
Movement Disorders Clinical Practice.2024; 11(3): 276. CrossRef
A meta-analysis of transcranial magnetic stimulation in Tourette syndrome
Elizabeth R. Steuber, Joseph F. McGuire
Journal of Psychiatric Research.2024; 173: 34. CrossRef
Premonitory Urge and Tic Severity, Comorbidities, and Quality of Life in Chronic Tic Disorders
Valerie Brandt, Jana Essing, Ewgeni Jakubovski, Kirsten Müller‐Vahl
Movement Disorders Clinical Practice.2023; 10(6): 922. CrossRef
Motor awareness, volition, and the cortical neurophysiology of simple motor tics
Aysegul Gunduz, Christos Ganos
Clinical Neurophysiology.2023; 151: 130. CrossRef
Tourette syndrome research highlights from 2022
Andreas Hartmann, Per Andrén, Cyril Atkinson-Clément, Virginie Czernecki, Cécile Delorme, Nanette Marinette Monique Debes, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Keisuke Ueda, Kevin J. Black
F1000Research.2023; 12: 826. CrossRef
Tourette syndrome research highlights from 2022
Andreas Hartmann, Per Andrén, Cyril Atkinson-Clément, Virginie Czernecki, Cécile Delorme, Nanette Marinette Monique Debes, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Keisuke Ueda, Kevin J. Black
F1000Research.2023; 12: 826. CrossRef
Door-To-Door Video-Enhanced Prevalence Study of Tourette Disorder Among African Americans
Catherine Striley, Kevin J. Black, Natalie E. Chichetto, Lauren Vagelakos
Evidence-Based Practice in Child and Adolescent Mental Health.2023; : 1. CrossRef
Clinical evaluation of premonitory urges in children and adolescents using the Chinese version of Individualized Premonitory Urge for Tics Scale
Guanghua Che, Wenjing Ren, Joseph F. McGuire, Ping Li, Zhiruo Zhao, Jing Tian, Jinyuan Zhang, Yue Zhang
Frontiers in Psychiatry.2023;[Epub] CrossRef
Mass social media-induced illness presenting with Tourette-like behavior
Carolin Fremer, Natalia Szejko, Anna Pisarenko, Martina Haas, Luise Laudenbach, Claudia Wegener, Kirsten R. Müller-Vahl
Frontiers in Psychiatry.2022;[Epub] CrossRef
Tics bei Erwachsenen
Tina Rawish, Gesine Sallandt, Alexander Münchau
NeuroTransmitter.2022; 33(12): 38. CrossRef

Fecal Calprotectin in Parkinson’s Disease and Multiple System Atrophy: Jia Wei Hor, Shen-Yang Lim, Eng Soon Khor, Kah Kian Chong, Sze Looi Song, Norlinah Mohamed Ibrahim, Cindy Shuan Ju Teh, Chun Wie Chong, Ida Normiha Hilmi, Ai Huey Tan; J Mov Disord. 2022;15(2):106-114. Published online December 24, 2021; DOI: https://doi.org/10.14802/jmd.21085

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Abstract PDF Supplementary Material

Objective
Converging evidence suggests that intestinal inflammation is involved in the pathogenesis of neurodegenerative diseases. Previous studies on fecal calprotectin in Parkinson’s disease (PD) were limited by small sample sizes, and literature regarding intestinal inflammation in multiple system atrophy (MSA) is very scarce. We investigated the levels of fecal calprotectin, a marker of intestinal inflammation, in PD and MSA.
Methods
We recruited 169 subjects (71 PD, 38 MSA, and 60 age-similar nonneurological controls). Clinico-demographic data were collected. PD and MSA were subtyped and the severity assessed using the MDS-UPDRS and UMSARS, respectively. Fecal calprotectin and blood immune markers were analyzed.
Results
Compared to controls (median: 35.7 [IQR: 114.2] μg/g), fecal calprotectin was significantly elevated in PD (median: 95.6 [IQR: 162.1] μg/g, p = 0.003) and even higher in MSA (median: 129.5 [IQR: 373.8] μg/g, p = 0.002). A significant interaction effect with age was observed; between-group differences were significant only in older subjects (i.e., ≥ 61 years) and became more apparent with increasing age. A total of 28.9% of MSA and 18.3% of PD patients had highly abnormal fecal calprotectin levels (≥ 250 μg/g); however, this difference was only significant for MSA compared to controls. Fecal calprotectin correlated moderately with selected blood immune markers in PD, but not with clinical features of PD or MSA.
Conclusions
Elevated fecal calprotectin suggests a role for intestinal inflammation in PD and MSA. A more complete understanding of gut immune alterations could open up new avenues of research and treatment for these debilitating diseases.

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Calprotectin in Parkinsonian disease: Anticipation and dedication
Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Ayah Talal Zaidalkiani, Athanasios Alexiou, Marios Papadakis, Mostafa M. Bahaa, Ammar AL-Faraga, Gaber El-Saber Batiha
Ageing Research Reviews.2024; 93: 102143. CrossRef
Diagnostic Accuracy of Fecal Calprotectin in Discriminating Organic-Inflammatory Gastrointestinal Diseases and Functional Gastrointestinal Disorders in Older Patients
Antonella Gallo, Marcello Covino, Silvia Baroni, Sara Camilli, Francesca Ibba, Silvia Andaloro, Maria Chiara Agnitelli, Fiammetta Maria Rognoni, Francesco Landi, Massimo Montalto
Journal of Personalized Medicine.2024; 14(3): 227. CrossRef
Nocardia cyriacigeorgica Elicits Gut Disturbances in a Leaky Gut Model of Colitis, but Not the Harmful Cascade Leading to Gut-First Parkinson’s Disease
João Duarte Magalhães, Emanuel Candeias, Inês Melo-Marques, António E. Abreu, Ana Raquel Pereira-Santos, Ana Raquel Esteves, Sandra Morais Cardoso, Nuno Empadinhas
International Journal of Molecular Sciences.2024; 25(6): 3423. CrossRef
Inflammation in multiple system atrophy
Marta Leńska-Mieciek, Natalia Madetko-Alster, Piotr Alster, Leszek Królicki, Urszula Fiszer, Dariusz Koziorowski
Frontiers in Immunology.2023;[Epub] CrossRef
Gut-to-brain spreading of pathology in synucleinopathies: A focus on molecular signalling mediators
Verena Schmitt, Rebecca Katharina Masanetz, Martin Weidenfeller, Lara Savannah Ebbinghaus, Patrick Süß, Stephan P. Rosshart, Stephan von Hörsten, Friederike Zunke, Jürgen Winkler, Wei Xiang
Behavioural Brain Research.2023; 452: 114574. CrossRef
Calprotectin, Biomarker of Depression in Patients with Inflammatory Bowel Disease?
Miorita Melina Iordache, Anca Mihaela Belu, Sabina E. Vlad, Kamer Ainur Aivaz, Andrei Dumitru, Cristina Tocia, Eugen Dumitru
Medicina.2023; 59(7): 1240. CrossRef
Different pieces of the same puzzle: a multifaceted perspective on the complex biological basis of Parkinson’s disease
Amica C. Müller-Nedebock, Marieke C. J. Dekker, Matthew J. Farrer, Nobutaka Hattori, Shen-Yang Lim, George D. Mellick, Irena Rektorová, Mohamed Salama, Artur F. S. Schuh, A. Jon Stoessl, Carolyn M. Sue, Ai Huey Tan, Rene L. Vidal, Christine Klein, Soraya
npj Parkinson's Disease.2023;[Epub] CrossRef
Fecal calprotectin as an intestinal inflammation marker is elevated in glaucoma
Zuo Wang, Hang Yuan, Xiong Zhu, Jinxia Wang, Wenbo Xiu, Yang Chen, Gao Zhang, Jing Fu, Kun Peng, An Li, Donghua Liu, Xijing Huang, Chong He, Fang Lu
Biomarkers in Medicine.2023; 17(9): 465. CrossRef
Pesticides and the Microbiome-Gut-Brain Axis: Convergent Pathways in the Pathogenesis of Parkinson’s Disease
Kristina Kulcsarova, Corinna Bang, Daniela Berg, Eva Schaeffer
Journal of Parkinson's Disease.2023; 13(7): 1079. CrossRef
The microbiome–gut–brain axis in Parkinson disease — from basic research to the clinic
Ai Huey Tan, Shen Yang Lim, Anthony E. Lang
Nature Reviews Neurology.2022; 18(8): 476. CrossRef
The Gut Microbiome–Brain Crosstalk in Neurodegenerative Diseases
Laura Ghezzi, Claudia Cantoni, Emanuela Rotondo, Daniela Galimberti
Biomedicines.2022; 10(7): 1486. CrossRef
Gastrointestinal Involvement in Extra-Digestive Disease: Which Is the Role of Fecal Calprotectin?
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Medicina.2022; 58(10): 1384. CrossRef

Review Articles

Treatable Ataxias: How to Find the Needle in the Haystack?: Albert Stezin, Pramod Kumar Pal; J Mov Disord. 2022;15(3):206-226. Published online September 7, 2022; DOI: https://doi.org/10.14802/jmd.22069

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Abstract PDF

Treatable ataxias are a group of ataxic disorders with specific treatments. These disorders include genetic and metabolic disorders, immune-mediated ataxic disorders, and ataxic disorders associated with infectious and parainfectious etiology, vascular causes, toxins and chemicals, and endocrinopathies. This review provides a comprehensive overview of different treatable ataxias. The major metabolic and genetic treatable ataxic disorders include ataxia with vitamin E deficiency, abetalipoproteinemia, cerebrotendinous xanthomatosis, Niemann-Pick disease type C, autosomal recessive cerebellar ataxia due to coenzyme Q10 deficiency, glucose transporter type 1 deficiency, and episodic ataxia type 2. The treatment of these disorders includes the replacement of deficient cofactors and vitamins, dietary modifications, and other specific treatments. Treatable ataxias with immune-mediated etiologies include gluten ataxia, anti-glutamic acid decarboxylase antibody-associated ataxia, steroid-responsive encephalopathy associated with autoimmune thyroiditis, Miller-Fisher syndrome, multiple sclerosis, and paraneoplastic cerebellar degeneration. Although dietary modification with a gluten-free diet is adequate in gluten ataxia, other autoimmune ataxias are managed by short-course steroids, plasma exchange, or immunomodulation. For autoimmune ataxias secondary to malignancy, treatment of tumor can reduce ataxic symptoms. Chronic alcohol consumption, antiepileptics, anticancer drugs, exposure to insecticides, heavy metals, and recreational drugs are potentially avoidable and treatable causes of ataxia. Infective and parainfectious causes of cerebellar ataxias include acute cerebellitis, postinfectious ataxia, Whipple’s disease, meningoencephalitis, and progressive multifocal leukoencephalopathy. These disorders are treated with steroids and antibiotics. Recognizing treatable disorders is of paramount importance when dealing with ataxias given that early treatment can prevent permanent neurological sequelae.

Citations

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Genetic Testing of Movements Disorders: A Review of Clinical Utility
Dennis Yeow, Laura I. Rudaks, Sue-Faye Siow, Ryan L. Davis, Kishore R. Kumar
Tremor and Other Hyperkinetic Movements.2024;[Epub] CrossRef
Rehabilitation in ataxia
Anupam Gupta, NavinB Prakash, Hafis Rahman
Indian Journal of Physical Medicine & Rehabilitation.2023; 33(1): 21. CrossRef

Evidence of Inflammation in Parkinson’s Disease and Its Contribution to Synucleinopathy: Thuy Thi Lai, Yun Joong Kim, Hyeo-il Ma, Young Eun Kim; J Mov Disord. 2022;15(1):1-14. Published online November 3, 2021; DOI: https://doi.org/10.14802/jmd.21078

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Abstract PDF

Accumulation of alpha-synuclein (αSyn) protein in neurons is a renowned pathological hallmark of Parkinson’s disease (PD). In addition, accumulating evidence indicates that activated inflammatory responses are involved in the pathogenesis of PD. Thus, achieving a better understanding of the interaction between inflammation and synucleinopathy in relation to the PD process will facilitate the development of promising disease-modifying therapies. In this review, the evidence of inflammation in PD is discussed, and human, animal, and laboratory studies relevant to the relationship between inflammation and αSyn are explored as well as new therapeutic targets associated with this relationship.

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Microglial inhibition alleviates alpha-synuclein propagation and neurodegeneration in Parkinson’s disease mouse model
Thuy Thi Lai, Young Eun Kim, Linh Thi Nhat Nguyen, Tinh Thi Nguyen, In Hee Kwak, Franziska Richter, Yun Joong Kim, Hyeo-il Ma
npj Parkinson's Disease.2024;[Epub] CrossRef
New Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases
Eveljn Scarian, Camilla Viola, Francesca Dragoni, Rosalinda Di Gerlando, Bartolo Rizzo, Luca Diamanti, Stella Gagliardi, Matteo Bordoni, Orietta Pansarasa
International Journal of Molecular Sciences.2024; 25(5): 2698. CrossRef
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Original Articles

Analysis of Semiology, Lesion Topography and Treatment Outcomes: A Prospective Study on Post Thalamic Stroke Holmes Tremor: Amlan Kusum Datta, Adreesh Mukherjee, Sudeshna Malakar, Atanu Biswas; J Mov Disord. 2024;17(1):71-81. Published online October 20, 2023; DOI: https://doi.org/10.14802/jmd.23095

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Abstract PDF Supplementary Material: Objective
Holmes tremor (HT) comprises rest, postural and intention tremor subtypes, usually involving both proximal and distal musculature. Perturbations of nigro-striatal pathways might be fundamental in the pathogenesis of HT along with cerebello-thalamic connections.
Methods
Nine patients with an HT phenotype secondary to thalamic stroke were included. Epidemiological and clinical records were obtained. Structural and functional brain imaging were performed with magnetic resonance imaging (MRI) or computed tomography (CT) and positron emission tomography (PET), respectively. Levodopa was administered in sequentially increasing dosage, with various other drugs in case of inadequate response. Longitudinal follow-up was performed for at least three months. The essential tremor rating assessment scale (TETRAS) was used for assessment.
Results
The mean latency from stroke to tremor onset was 50.4 ± 30.60 days (range 21–90 days). Dystonia was the most frequently associated hyperkinetic movement (88.8%). Tremor was bilateral in 22.2% of participants. Clinical response was judged based on a reduction in the TETRAS score by a prefixed value (≥ 30%), pertaining to which 55.5% (n = 5) of subjects were classified as responders and the rest as non-responders. The responders showed improvement with significantly lower doses of levodopa than the remaining nonresponders (240 ± 54.7 mg vs. 400 ± 40.8 mg; p = 0.012).
Conclusion
Although levodopa is useful in HT, augmenting the dosage of levodopa beyond a certain point might not benefit patients clinically. Topography of vascular lesions within the thalamus might additionally influence the phenomenology of HT.

Comparative Olfactory Profiles in Parkinson’s Disease and Drug-Induced Parkinsonism: In Hee Kwak, Young Eun Kim, Suk Yun Kang, Joong Seob Lee, Jeongjae Lee, Min Seung Kim, Dong A Yea, Hyeo-il Ma; J Mov Disord. 2024;17(1):64-70. Published online October 6, 2023; DOI: https://doi.org/10.14802/jmd.23105

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Abstract PDF Supplementary Material: Objective
Drug-induced parkinsonism (DIP) is a frequently encountered diagnostic possibility when considering Parkinson’s disease (PD). While olfactory dysfunction is a common clinical feature in PD, the comparison of olfactory function between the two conditions remains insufficient. This study aimed to compare olfactory function, including threshold, discrimination, and identification (TDI) profiles, between PD and DIP.
Methods
Consecutive patients with drug-naïve PD (n = 78) or DIP (n = 31) confirmed through dopamine transporter imaging were enrolled in this study. The YSK olfactory function (YOF) test, composed of TDI domains culturally familiar odorants to Koreans, was administered to all patients.
Results
In the study population, patients with DIP were significantly older than patients with PD. Over 70% of patients in each group had hyposmia or anosmia, and there was no significant difference in the occurrence of olfactory dysfunction between the two groups. In addition, there were no differences in the total YOF score and threshold score between the two groups. Meanwhile, the PD group had a significantly lower discrimination and identification score than the DIP group after adjusting for age, sex, the existence of diabetes, disease duration, and cognitive function.
Conclusion
This study demonstrated that detailed olfactory profiles are different in PD and DIP, even though olfactory dysfunction can be observed in both conditions.

Retinal Thinning as a Marker of Disease Severity in Progressive Supranuclear Palsy: Yueting Chen, Haotian Wang, Bo Wang, Wenbo Li, Panpan Ye, Wen Xu, Peng Liu, Xinhui Chen, Zhidong Cen, Zhiyuan Ouyang, Sheng Wu, Xiaofeng Dou, Yi Liao, Hong Zhang, Mei Tian, Wei Luo; J Mov Disord. 2024;17(1):55-63. Published online September 26, 2023; DOI: https://doi.org/10.14802/jmd.23102

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Abstract PDF Supplementary Material

Objective
Progressive supranuclear palsy (PSP) involves a variety of visual symptoms that are thought to be partially caused by structural abnormalities of the retina. However, the relationship between retinal structural changes, disease severity, and intracranial alterations remains unknown. We investigated distinct retinal thinning patterns and their relationship with clinical severity and intracranial alterations in a PSP cohort.
Methods
We enrolled 19 patients with PSP (38 eyes) and 20 age-matched healthy controls (40 eyes). All of the participants underwent peripapillary and macular optical coherence tomography. Brain ¹¹C-2β-carbomethoxy-3β-(4-fluorophenyl) tropane (¹¹C-CFT) and ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography imaging were also performed in patients with PSP. We investigated the association between retinal thickness changes and clinical features, striatal dopamine transporter availability, and cerebral glucose metabolism.
Results
The peripapillary retinal nerve fiber layer (pRNFL) and macula were significantly thinner in patients with PSP than in controls. The thickness of the superior sector of the pRNFL demonstrated a significant negative relationship with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale part III and Hoehn and Yahr staging scale scores. A significant negative correlation was found between outer inferior macular thickness and disease duration. Outer temporal macular thickness was positively correlated with Montreal Cognitive Assessment scores. In PSP, lower outer temporal macular thickness was also positively correlated with decreased dopamine transporter binding in the caudate.
Conclusion
The pRNFL and macular thinning may be candidate markers for monitoring disease severity. Additionally, macular thinning may be an in vivo indicator of nigrostriatal dopaminergic cell degeneration in PSP patients.

Citations

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Optical Coherence Tomography as a Biomarker in the Differential Diagnosis between Parkinson’s Disease and Atypical Parkinsonian Syndromes: A Narrative Review
Stella Karatzetzou, Dimitrios Parisis, Serafeim Ioannidis, Theodora Afrantou, Panagiotis Ioannidis
Applied Sciences.2024; 14(6): 2491. CrossRef

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