Oyedele J Olaoye, Sophie L Farrow, Denis M Nyaga, Antony A Cooper, Justin M O'Sullivan
{"title":"From blood vessels to brain cells: Connecting the circulatory system and Parkinson's disease.","authors":"Oyedele J Olaoye, Sophie L Farrow, Denis M Nyaga, Antony A Cooper, Justin M O'Sullivan","doi":"10.1177/1877718X241308168","DOIUrl":"10.1177/1877718X241308168","url":null,"abstract":"<p><p>Parkinson's disease (PD) is traditionally recognized as a neurodegenerative disorder characterized by motor dysfunction and α-synuclein protein accumulation in the brain. However, recent research suggests that the circulatory system may also contribute to PD pathogenesis through the spread of α-synuclein beyond the brain. The blood-brain barrier (BBB), a key regulator of molecular exchange between the bloodstream and the brain, may become compromised in PD, allowing harmful substances, including pathogenic forms of α-synuclein, to infiltrate the brain and promote neurodegeneration. Transport mechanisms such as P-glycoprotein and the low-density lipoprotein (LDL) receptor-related protein (LRP-1) further modulate the movement of α-synuclein across the BBB, influencing disease progression. Additionally, extracellular vesicles are emerging as crucial mediators in the dissemination of α-synuclein between the brain and peripheral tissues, facilitating its spread and accumulation. The lymphatic system, responsible for clearing α-synuclein, may also contribute to PD pathology when impaired. This review highlights the growing evidence for a circulatory axis in the initiation and progression of PD. We propose that future research should explore the hypothesis that the circulatory system contributes to the pathogenesis of PD by aiding the distribution of α-synuclein throughout the body.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"255-268"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sinah Röttgen, Marie-Sophie Lindner, Aline Seger, Johanna Kickartz, Kim-Lara Weiß, Christopher Ej Doppler, Gereon R Fink, Anja Ophey, Michael Sommerauer
{"title":"Non-motor symptoms in prodromal Parkinson's disease are linked to reduced quality of life.","authors":"Sinah Röttgen, Marie-Sophie Lindner, Aline Seger, Johanna Kickartz, Kim-Lara Weiß, Christopher Ej Doppler, Gereon R Fink, Anja Ophey, Michael Sommerauer","doi":"10.1177/1877718X241310726","DOIUrl":"10.1177/1877718X241310726","url":null,"abstract":"<p><p>Isolated rapid eye movement (REM) sleep behavior disorder (iRBD) highlights an early α-synucleinopathy. This study compared health-related quality of life (hrQoL) in 62 individuals with iRBD with 19 healthy controls (HC) and 29 individuals with Parkinson's disease (PD) and identified factors linked to poorer hrQoL. HrQoL was significantly lower in individuals with iRBD (83.33 ± 16.96) compared to HC (92.29 ± 5.49, p = 0.027). Poorer hrQoL in individuals with iRBD was linked to severity of multiple non-motor symptoms, most prominently fatigue and depressive symptoms being significant predictors (<i>p </i>< 0.001, adjusted <i>R</i><sup>2</sup> = 0.81). This study highlights the importance of non-motor symptoms for hrQoL in prodromal PD.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"434-439"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guillaume Carey, Mark L Kuijf, Stijn Michielse, Amée F Wolters, Kathy Dujardin, Albert Fg Leentjens
{"title":"Reduced volume of the mediodorsal and anteroventral thalamus is associated with anxiety in Parkinson's disease: A cross-sectional 7-tesla MRI study.","authors":"Guillaume Carey, Mark L Kuijf, Stijn Michielse, Amée F Wolters, Kathy Dujardin, Albert Fg Leentjens","doi":"10.1177/1877718X241308141","DOIUrl":"10.1177/1877718X241308141","url":null,"abstract":"<p><p>BackgroundParkinson's disease (PD)-related anxiety occurs frequently and may be associated with imbalance between anxiety-related circuits. While the thalamus is a shared region of these circuits, its role in PD-related anxiety has not been explored so far.ObjectiveTo identify changes in volume of the thalamus and its subnuclei in patients with PD-related anxiety.MethodsCognitively intact PD patients (n = 105) were divided into two groups based on their score on the Parkinson anxiety scale (PAS): 31 PD patients had anxiety (Anx-PD) and 74 did not have anxiety (non-Anx-PD). Forty-five healthy control subjects were included. Participants underwent 7-Tesla MRI scanning. Using automatic segmentation, the volumes of the thalamus and its subnuclei were measured, compared between the groups and regressed on the PAS.ResultsThe volumes of the thalamus and its subnuclei did not significantly differ between the groups. However, in anxious PD patients, more severe anxiety was strongly associated with a smaller volume of the right medial thalamic subregion, specifically the right mediodorsal magnocellular nucleus and the right mediodorsal parvocellular nucleus (R = 0.63, ß<sub>PAS </sub>= -0.546, p-value<sub>model </sub>= 0.007 and R = 0.60, ß<sub>PAS </sub>= -0.547, p-value<sub>model </sub>= 0.016, respectively), and of the left anteroventral thalamus (R = 0.73, FDR p-value<sub>model </sub>= 0.002, ß<sub>PAS </sub>= -0.407, p-value<sub>PAS </sub>= 0.01).ConclusionsA reduced volume of the mediodorsal and anteroventral thalamus, overlapping structures between the anxiety related circuits, are associated with more severe PD-related anxiety and may explain its high prevalence in the disease.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"338-348"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christopher Käufer, Miloš Stanojlović, Alina Schidlitzki, Jana Bonsberger, Alexander Storch, Franziska Richter
{"title":"Alterations in non-REM sleep and EEG spectra precede REM-sleep deficits in a model of synucleinopathy.","authors":"Christopher Käufer, Miloš Stanojlović, Alina Schidlitzki, Jana Bonsberger, Alexander Storch, Franziska Richter","doi":"10.1177/1877718X241310723","DOIUrl":"10.1177/1877718X241310723","url":null,"abstract":"<p><p>BackgroundSleep disturbances often precede motor symptoms in neurodegenerative diseases like Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Neuroinflammation is implicated in PD pathophysiology and may contribute to non-motor symptoms such as sleep disturbances. The Thy1-αSyn mouse model, overexpressing human alpha-synuclein (αSyn), mimics key aspects of PD and DLB, making it valuable for studying related sleep disturbances and neuroinflammatory changes.ObjectiveTo investigate early-stage alterations in sleep architecture, electroencephalographic (EEG) patterns, and neuroinflammation in Thy1-αSyn mice.MethodsWe used telemetric EEG/electromyography (EMG) with video surveillance to compare sleep patterns and EEG spectral power between 2.5- and 4.5-month-old male Thy1-αSyn transgenic mice and wild-type littermates. Neuroinflammation was assessed by examining microglial (Iba1) and astrocytic (GFAP) activation in key sleep-regulating brain regions.ResultsThy1-αSyn mice showed decreased resting wake time and increased non-REM sleep, with altered sleep bout frequency and length, indicating significant sleep architecture changes. Spectral analysis revealed a shift from higher to lower frequency bands, suggesting early neural circuitry disruptions due to αSyn overexpression. Significant microglial activation was observed at 3 months, with astrogliosis progressing by 5 months in key sleep-regulating regions, indicating that neuroinflammation may contribute to the observed sleep disturbances.ConclusionsEarly-stage Thy1-αSyn mice exhibit significant sleep architecture changes, EEG spectral shifts, and neuroinflammatory alterations. These findings suggest that neuroinflammation may play a role in the initial pathophysiological changes in PD and related synucleinopathies. Sleep, EEG, and neuroinflammatory changes could serve as early biomarkers for these diseases.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"311-328"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Improving reliability of movement assessment in Parkinson's disease using computer vision-based automated severity estimation.","authors":"Jinyu Xu, Xin Xu, Xudong Guo, Zezhi Li, Boya Dong, Chen Qi, Chunhui Yang, Dong Zhou, Jiali Wang, Lu Song, Ping He, Shanshan Kong, Shuchang Zheng, Sichao Fu, Wei Xie, Xuan Liu, Ya Cao, Yilin Liu, Yiqing Qiu, Zhiyuan Zheng, Fei Yang, Jing Gan, Xi Wu","doi":"10.1177/1877718X241312605","DOIUrl":"10.1177/1877718X241312605","url":null,"abstract":"<p><p>BackgroundClinical assessments of motor symptoms rely on observations and subjective judgments against standardized scales, leading to variability due to confounders. Improving inter-rater agreement is essential for effective disease management.ObjectiveWe developed an objective rating system for Parkinson's disease (PD) that integrates computer vision (CV) and machine learning to correct potential discrepancies among raters while providing the basis for model performance to gain professional acceptance.MethodsA prospective PD cohort (n = 128) were recruited from multi-centers. Motor examination videos were recorded using an android tablet with CV-based software following the MDS-UPDRS Part-III instructions. Videos included facial, upper- and lower-limb movements, arising from a chair, standing, and walking. Fifteen certified clinicians were recruited from multi-centers. For each video, five clinicians were randomly selected to independently rate the severity of motor symptoms, validate the videos and movement variables (MovVars). Machine learning algorithms were applied for automated rating and feature importance analysis. Inter-rater agreement among human raters and the agreement between artificial intelligence (AI)-generated ratings and expert consensus were calculated.ResultsFor all validated videos (n = 1024), AI-based ratings showed an average absolute accuracy of 69.63% and an average acceptable accuracy of 98.78% against the clinician consensus. The mean absolute error between the AI-based scores and clinician consensus was 0.32, outperforming the inter-rater variability (0.65), potentially due to the combined utilization of diverse MovVars.ConclusionsThe algorithm enabled accurate video-based evaluation of mild motor symptom severity. AI-assisted assessment improved the inter-rater agreement, demonstrating the practical value of CV-based tools in screening, diagnosing, and treating movement disorders.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"349-360"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stuart H Isaacson, Alberto J Espay, Rajesh Pahwa, Pinky Agarwal, Holly A Shill, Jennifer Hui, Khashayar Dashtipour, Mark Lew, Peibing Qin, Andrea E Formella, Gianpiera Ceresoli-Borroni, Peter A LeWitt
{"title":"Continuous, subcutaneous apomorphine infusion for Parkinson disease motor fluctuations: Results from the phase 3, long-term, open-label United States InfusON study.","authors":"Stuart H Isaacson, Alberto J Espay, Rajesh Pahwa, Pinky Agarwal, Holly A Shill, Jennifer Hui, Khashayar Dashtipour, Mark Lew, Peibing Qin, Andrea E Formella, Gianpiera Ceresoli-Borroni, Peter A LeWitt","doi":"10.1177/1877718X241310727","DOIUrl":"10.1177/1877718X241310727","url":null,"abstract":"<p><p>BackgroundContinuous subcutaneous apomorphine infusion (CSAI) has been used globally since the 1980s for Parkinson disease (PD) motor fluctuations but has not been available in the United States (US).ObjectiveEvaluate CSAI for motor fluctuations in the US setting.MethodsThis open-label study (NCT02339064) enrolled patients with PD experiencing ≥3 hours (h) daily OFF time despite optimized levodopa and current/prior use of at least one other adjunctive therapy. CSAI was initiated with a 1-2 mg bolus followed by 1 mg/h infusion titrated to optimal efficacy and tolerability. Following titration, patients entered a 52-week maintenance period.ResultsOf 99 patients treated, 85 completed the titration period, 69 completed maintenance week 12 and 48 completed maintenance week 52. Common treatment-related adverse events included infusion site nodules and erythema, dyskinesia, nausea, and somnolence, each of which occurred more frequently during the titration period. Reduction in OFF time began at CSAI initiation and reached a mean of 3.0 ± 3.18 h/day by maintenance week 12 (primary efficacy endpoint), with a corresponding increase in Good ON time of 3.1 ± 3.35 h/day. By maintenance week 12, 68% of patients rated themselves as much or very much improved, 62% had at least a 2-h reduction in daily OFF time, and mean concomitant oral levodopa and levodopa equivalent doses (excluding CSAI) had been reduced by 198 mg/day and 283 mg/day, respectively. Improvements were maintained through week 52.ConclusionsThis study supports the clinical utility of CSAI to reduce OFF time and increase Good ON time in patients with motor fluctuations inadequately controlled with oral therapy.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"361-373"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kátia Cirilo Costa Nóbrega, Isaíra Almeida Pereira da Silva Nascimento, Bruno Rafael Antunes Souza, Raíssa Amorim Gonçalves, Thalyta Silva Martins, Geovanna Ferreira Santos, Bruno Eron de Almeida da Silva, André Helene Frazão, Antônio Carlos Roque, Rodolfo Savica, Maria Elisa Pimentel Piemonte
{"title":"The impact of motor, non-motor, and social aspects on the sexual health of women living with Parkinson's disease.","authors":"Kátia Cirilo Costa Nóbrega, Isaíra Almeida Pereira da Silva Nascimento, Bruno Rafael Antunes Souza, Raíssa Amorim Gonçalves, Thalyta Silva Martins, Geovanna Ferreira Santos, Bruno Eron de Almeida da Silva, André Helene Frazão, Antônio Carlos Roque, Rodolfo Savica, Maria Elisa Pimentel Piemonte","doi":"10.1177/1877718X251315375","DOIUrl":"10.1177/1877718X251315375","url":null,"abstract":"<p><p>BackgroundSexual health is influenced by a complex interplay of biological, psychological, and social factors, all of which can be impacted by Parkinson's disease (PD). Female sexual dysfunction includes reduced sexual desire and/or arousal, pain during sexual activity, or difficulty achieving orgasm. Despite its impact on quality of life, sexual health in women with PD remains poorly understood.ObjectiveTo investigate the impact of motor, non-motor, and social PD aspects on sexual health of women with PD.MethodsWe conducted a cross-sectional study with 100 women with PD (Hoehn and Yahr stages 1-3) who reported an active sex life in the last six months. Data were collected via remote interviews and included demographic and clinical features, cognitive capacity, motor and non-motor experiences, fatigue, self-esteem, sleep disorders, couple relationship quality, depressive symptoms, and sexual health assessments using the Female Sexual Function Index (FSFI) and Sexual Quotient-Female (SQ-F). Multiple regression models were used to identify predictors of FSFI and SQ-F scores.ResultsResults indicated that while several motor, non-motor, and social factors correlated with sexual health, only couple relationship quality and sleep quality significantly predicted both short-term (FSFI) and long-term (SQ-F) sexual health. No significant associations were observed with age, disease onset, postmenopausal status, or daily medication dosage.ConclusionsThe present study's evidence identifies multiple key areas, such as couple's relationship quality and sleep quality that could be targeted for intervention to improve sexual health in women with PD.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"421-433"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Orly Goldstein, Shachar Shani, Mali Gana-Weisz, Nadav Elkoshi, Fergal Casey, Yu H Sun, Khyati Chandratre, Jesse M Cedarbaum, Cornelis Blauwendraat, Anat Bar-Shira, Avner Thaler, Tanya Gurevich, Anat Mirelman, Nir Giladi, Avi Orr-Urtreger, Roy N Alcalay
{"title":"The effect of polygenic risk score on PD risk and phenotype in <i>LRRK2</i> G2019S and <i>GBA1</i> carriers.","authors":"Orly Goldstein, Shachar Shani, Mali Gana-Weisz, Nadav Elkoshi, Fergal Casey, Yu H Sun, Khyati Chandratre, Jesse M Cedarbaum, Cornelis Blauwendraat, Anat Bar-Shira, Avner Thaler, Tanya Gurevich, Anat Mirelman, Nir Giladi, Avi Orr-Urtreger, Roy N Alcalay","doi":"10.1177/1877718X241310722","DOIUrl":"10.1177/1877718X241310722","url":null,"abstract":"<p><p>BackgroundWhile <i>LRRK2</i> and <i>GBA1</i> variants are associated with Parkinson's disease (PD), most carriers will not develop the disease.ObjectiveTo test if polygenic risk score (PRS) modifies disease risk and phenotypes in <i>LRRK2</i> G2019S carriers, <i>GBA1</i> carriers, and non-carriers (NC).MethodsWe genotyped 786 participants using Illumina's NeuroBooster-array (NBA) and sequenced the genome of 244, all of Ashkenazi ancestry (AJ), and calculated PRS to test its effects on clinically- and biologically-defined disease risk and phenotypes (n = 715). Among <i>LRRK2</i> G2019S PD, we tested PRS association with α-synuclein seed-amplification-assay (n = 11). We used the PPMI and AMP-PD databases as validation cohorts.ResultsIn clinically-defined PD, PRS significantly modified disease risk in <i>GBA1</i> carriers and in NC (<i>p </i>= 0.033 and <i>p </i>< 0.0001, respectively), and demonstrated a trend in <i>LRRK2</i> G2019S carriers (<i>p </i>= 0.054), with similar effect sizes (OR = 1.55, 1.62, and 1.49, respectively). PRS association with PD risk in <i>LRRK2</i> was primarily driven by the rs7938782-A risk allele, replicated in AMP-PD (268 AJs <i>LRRK2</i> G2019S carriers). PRS and age-at-onset were negatively correlated in NC (<i>p </i>< 0.0001). NBA <i>GBA1</i> genotype calls failed at <i>GBA1</i> L483P and c.115 + 1G > A mutations. False negative call rate of 10.2% was observed for the imputed <i>GBA1</i> N409S carriers.ConclusionsPRS contributes to PD risk across different genotypes. The genetic and epigenetic role of rs7938782 in <i>LRRK2</i> PD risk should be further explored. Future PRS models should be tailored to specific genotypes to better understand penetrance and phenotypes. Furthermore, models predicting PD defined biologically rather than clinically may further identify genetic risk factors for synucleinopathies.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"291-299"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aging, cellular senescence and Parkinson's disease.","authors":"Yue Ma, Madalynn L Erb, Darren J Moore","doi":"10.1177/1877718X251316552","DOIUrl":"10.1177/1877718X251316552","url":null,"abstract":"<p><p>Parkinson's disease (PD) is the most common neurodegenerative movement disorder, affecting 1-2% of people over age 65. The risk of developing PD dramatically increases with advanced age, indicating that aging is likely a driving factor in PD neuropathogenesis. Several age-associated biological changes are also hallmarks of PD neuropathology, including mitochondrial dysfunction, oxidative stress, and neuroinflammation. Accumulation of senescent cells is an important feature of aging that contributes to age-related diseases. How age-related cellular senescence affects brain health and whether this phenomenon contributes to neuropathogenesis in PD is not yet fully understood. In this review, we highlight hallmarks of aging, including mitochondrial dysfunction, loss of proteostasis, genomic instability and telomere attrition in relation to well established PD neuropathological pathways. We then discuss the hallmarks of cellular senescence in the context of neuroscience and review studies that directly examine cellular senescence in PD. Studying senescence in PD presents challenges and holds promise for advancing our understanding of disease mechanisms, which could contribute to the development of effective disease-modifying therapeutics. Targeting senescent cells or modulating the senescence-associated secretory phenotype (SASP) in PD requires a comprehensive understanding of the complex relationship between PD pathogenesis and cellular senescence.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"239-254"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jamie Af Jansen, Tom Jw Buurke, Lotte van de Venis, Vivian Weerdesteyn, Noël Keijsers, Jorik Nonnekes
{"title":"Narrow-based gait in people with Parkinson's disease: Its mechanisms explored.","authors":"Jamie Af Jansen, Tom Jw Buurke, Lotte van de Venis, Vivian Weerdesteyn, Noël Keijsers, Jorik Nonnekes","doi":"10.1177/1877718X241313333","DOIUrl":"10.1177/1877718X241313333","url":null,"abstract":"<p><p>BackgroundPeople with Parkinson's disease (PD) typically exhibit a narrow-based gait. We previously found that walking with reduced trunk rotation and obliquity led to narrow-based gait in healthy adults; a decrease in trunk motion coincided with a decrease in mediolateral extrapolated center of mass (XCoM) excursion, requiring a smaller step width to maintain a constant mediolateral margin of stability (MoS).ObjectiveTo assess whether reduced trunk motion in PD is related to narrow-based gait, without affecting mediolateral MoS. To explore the underlying mechanisms of narrow-based gait, we examined the effects of increasing arm swing (aiming to increase trunk motion), and widening steps on gait in PD.MethodsFifteen people with PD and narrow-based gait and 17 age-matched controls walked on a treadmill for three minutes at a fixed gait speed during three conditions: baseline, increased arm swing and widened step width. Step width, trunk rotation and obliquity were calculated using marker data, and XCoM excursion and MoS using ground reaction forces.ResultsTrunk rotation, XCoM excursion, and step width were significantly smaller in PD compared to controls, while the MoS did not differ. Increased arm swing did not substantially increase trunk motions in PD, though people with PD were able to widen their step width.ConclusionsWe provide further evidence for a relation between trunk motion and step width. In PD, reduced trunk motion may contribute to narrow-based gait, without affecting mediolateral MoS; future work is needed to confirm a causal relationship between reduced trunk motion and narrow-based gait in PD.</p>","PeriodicalId":16660,"journal":{"name":"Journal of Parkinson's disease","volume":" ","pages":"329-337"},"PeriodicalIF":4.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}