Parkinson's disease (PD) is a neurodegenerative disorder primarily characterized by motor symptoms, including bradykinesia, rigidity, and resting tremor. PD is also accompanied by numerous non-motor symptoms, including sensory abnormalities, behavioral changes, sleep disturbances, and autonomic dysfunction such as orthostatic hypotension, bladder dysfunction and gastrointestinal dysfunction (including drooling, dysphagia and constipation). Drooling is one of the most common symptoms, negatively impacting oral health. It significantly affects physical well-being, psychological well-being, and quality of life for patients and their caregivers. This review aims to explore the mechanisms underlying drooling in PD, including its epidemiology, pathophysiology, and contributing factors. It also seeks to raise awareness and summarize current treatment strategies to improve patient outcomes.

The white matter pathology in Parkinson's disease with REM sleep behavior disorder (PD-RBD) and its link to sleep disturbances remain poorly understood. In this study, advanced diffusion MRI techniques, including diffusion kurtosis imaging (DKI) and neurite orientation dispersion and density imaging (NODDI), were used to characterize microstructural integrity within the corpus callosum and key limbic white matter tracts in PD-RBD patients. The results revealed that DKI metrics, specifically fractional anisotropy (FA) and mean kurtosis (MK) in the corpus callosum and cingulate, were significantly higher in the PD-nRBD group than in both the PD-RBD and healthy controls, with no significant differences between PD-RBD and HCs. Furthermore, Epworth Sleepiness Scale (ESS) scores were negatively correlated with the MK value in the right cingulate in PD-RBD patients. We speculate that, as the disease progresses, their microstructural alterations may reflect a transition from compensation to decompensation, with changes in these regions serving as potential neuroimaging markers of early disease progression.

Background: Growing evidence suggests that urinary β-amyloid precursor protein (AβPP) fragments can serve as an early screening biomarker for mild cognitive impairment and dementia. However, in reality, older adults, regardless of the presence of cognitive decline, often suffer from multiple age-related conditions and are on multiple medications. How these comorbidities and treatments affect the performance of early diagnostic biomarkers remains unclear. Methods : This study further validated the sensitivity, specificity, and clinical value of the Qankorey ® urinary β-amyloid protein detection kit in early dementia screening through a randomized community screening (n=51187) conducted in Changsha, and a multicenter case-control study conducted at Yuquan Hospital (Tsinghua University), Tiantan Hospital (Capital Medical University), Beijing Friendship Hospital, Zibo 148 Hospital (Shandong), and the Third People's Hospital of Yunnan Province. The multicenter case-control study included 898 participants, comprising 266 healthy, age-matched controls without any comorbidities, 167 patients with mild cognitive impairment/Alzheimer's disease (MCI/AD), and 465 non-AD patients with various comorbidities and age-related diseases. Results: The kit showed a significant age-dependent positive rate in both men and women in Changsha, increasing from 6.29% to 15.40%. The number of weakly positive/positive/negative individuals in the healthy group, non-AD group, and MCI/AD group were 8/12/246 (positive rate 7.52%), 41/16/409 (12.23%), and 77/44/46 (72.46%), respectively, with a Kappa value of 0.669, indicating that the method performed well in the clinical diagnosis of MCI/AD, consistent with previously published results. Among the 8 weakly positive healthy subjects, 6 were found to have brain abnormalities by MRI/CT examination. Comorbidity analysis showed that memory decline was the most significant risk factor (P=9.6 × 10^-23, Fisher's exact test), followed by dizziness (P=1.3 × 10^-14;) , hyperlipidemia (P=3.2 × 10^-12) , history of stroke (P=0.0011), and hypertension (P=0.0058). Treatment analysis showed that cardiovascular drugs and antithrombotic drugs significantly reduced the risk of dementia (P values were 0.0061 and 0.0081, respectively), followed by hypoglycemic drugs (P=0.0358). For AD patients, those receiving only memantine showed a slightly lower positive test rate (P=0.0532). Conclusion: Our findings confirm the diagnostic value of urinary β-amyloid protein detection in MCI and AD-related dementia. Furthermore, this kit can be used in practical clinical applications to assess the risk of cognitive decline and treatment efficacy across various diseases. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study did not receive any funding ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Ethics Committee of Yuquan Hospital of Tsinghua University gave ethical approval for this work. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors

Rapid eye movement sleep behavior disorder (RBD) is characterized by the loss of muscle atonia during rapid eye movement (REM) sleep, leading to the enactment of vivid and often unpleasant dreams. Studies have shown that it is closely related to alpha-synuclein neurodegenerative diseases, particularly Parkinson's disease (PD) and dementia with Lewy bodies (DLB). RBD serves not merely as an early warning signal but also is a manifestation of the pathogenesis of PD. Therefore, elucidating the pathological mechanisms underlying RBD is essential for enhancing the accuracy of early diagnosis and developing effective treatments for PD and DLB. Animal models remain fundamental in this research, enabling the exploration of specific pathophysiological traits, behavioral phenotypes, and potential therapeutic interventions. This review synthesizes recent advances in RBD modeling, including methodologies for model construction, core pathological mechanisms, and associated behavioral phenotypes. By examining the limitations of existing paradigms and proposing new avenues for research, we aim to provide a deeper insight into the mechanistic link between RBD and parkinsonian pathology.

Previous research has commonly regarded overactive bladder syndrome (OAB) and restless legs syndrome (RLS) as distinct disorders in terms of their underlying causes, clinical diagnosis, and treatment approaches. However, there is evidence of an overlap in the occurrence of these two conditions following cerebral infarction(CI). Specifically, restless bladder syndrome (RBS), a subtype of RLS, exhibits symptoms similar to those of OAB. Consequently, further investigation is warranted to better understand the relationship between these two disorders. In this report, we present the cases of two patients who presented with both OAB following CI, along with RLS. Following administration of oral pramipexole, both nocturia and RLS exhibited prompt and efficient alleviation. There may exist a shared pathological foundation between certain RLS cases and OAB. In instances where patients exhibit evident OAB symptoms following CI and concurrently experience RLS, it is advisable to prioritize the administration of dopaminergic agonists over M receptor inhibitors and β3 agonists. Furthermore, it is plausible that the RBS or a subset of RLS cases could potentially be classified as a form of OAB, although this correlation has yet to be definitively established.

Background::Gait impairment is closely related to quality of life in patients with Parkinson’s disease (PD). This study aimed to explore alterations in brain microstructure in PD patients and healthy controls (HCs) and to identify the correlation of gait impairment in the ON and OFF states of patients with PD, respectively.Methods::We enrolled 24 PD patients and 29 HCs from the Movement Disorders Program at Beijing Friendship Hospital Capital Medical University between 2019 and 2020. We acquired magnetic resonance imaging (MRI) scans and processed the diffusion kurtosis imaging (DKI) images. Preprocessing of diffusion-weighted data was performed with Mrtrix3 software, using a directional distribution function to track participants’ main white matter fiber bundles. Demographic and clinical characteristics were recorded. Quantitative gait and clinical scales were used to assess the status of medication ON and OFF in PD patients.Results::The axial kurtosis (AK), mean kurtosis (MK), and radial kurtosis (RK) of five specific white matter fiber tracts, the bilateral corticospinal tract, left superior longitudinal fasciculus, left anterior thalamic radiation, forceps minor, and forceps major were significantly higher in PD patients compared to HCs. Additionally, the MK values were negatively correlated with Timed Up and Go Test (TUG) scores in both the ON and OFF in PD patients. Within the PD group, higher AK, MK, and RK values, whether the patients were ON or OFF, were associated with better gait performance (i.e., higher velocity and stride length).Conclusions::PD exhibits characteristic regional patterns of white matter microstructural degradation. Correlations between objective gait parameters and DKI values suggest that dopamine-responsive gait function depends on preserved white matter microstructure. DKI-based Tract-Based Spatial Statistics (TBSS) analysis may serve as a tool for evaluating PD-related motor impairments (e.g., gait impairment) and could yield potential neuroimaging biomarkers.

Parkinson’s disease (PD) and type 2 diabetes mellitus (T2DM) exhibit increasing comorbidity, yet the shared contribution of gut microbiota remains unclear. To investigate parallel microbial and functional alterations underlying PD, T2DM, and PD with diabetes (PDDM), we performed fecal metagenomic sequencing in 156 PD, 41 T2DM, and 44 PD with diabetes (PDDM) patients and 83 healthy controls (HC). PD and T2DM showed highly concordant microbial shifts, with 22 genera and 91 species consistently altered across disease groups compared with HC. Functional enrichment highlighted common perturbations in taurine and hypotaurine metabolism, retinol metabolism, the hypoxia-inducible factor-1 (HIF-1) pathway, and xenobiotic degradation, implicating disrupted oxidative stress responses, neuro-metabolic regulation, and detoxification. Key taxa, including Limosilactobacillus fermentum, Lactobacillus porci, and Lactobacillus delbrueckii, were increased and showed moderate positive correlations (|ρ| ≥ 0.3) with antioxidant/retinol–HIF-1, taurine–hypotaurine, and xenobiotic degradation pathways. Bifidobacterium breve (unadjusted analysis) was increased in PD and further enriched in PDDM, correlating with multiple beneficial pathways. Bifidobacterium simiarum (covariate-adjusted analyses) showed the broadest positive pathway associations, while selected Bacteroides species (e.g., B. acidifaciens) exhibited negative correlations with insulin-resistance pathways and positive correlations with steroid hormone biosynthesis. By contrast, Butyricimonas vaginalis showed negative correlations with HIF-1 and insulin signaling and with cytochrome P450-related drug metabolism. These findings provide the first systematic evidence of parallel taxonomic and functional dysbiosis in PD and T2DM, supporting gut microbiota as a shared mediator and potential therapeutic target in comorbidity.

Emerging evidence suggests that dysbiosis of the gut microbiota is associated with the pathogenesis of Parkinson’s disease (PD), a prevalent neurodegenerative disorder. The microbiota-gut-brain axis plays a crucial role in the development and progression of PD, and numerous studies have demonstrated the potential therapeutic benefits of modulations in the intestinal microbiota. This review provides insights into the characterization of the gut microbiota in patients with PD and highlights associations with clinical symptoms and underlying mechanisms. The discussion underscores the increased influence of the gut microbiota in the pathogenesis of PD. While the relationship is not fully elucidated, existing research demonstrates a strong correlation between changes in the composition of gut microbiota and disease development, and further investigation is warranted to explain the specific underlying mechanisms.

Essential tremor (ET) is a highly prevalent movement disorder characterized by high heritability. However, the genetic basis of this disease remains largely unknown. Understanding the genetic causes of ET is crucial for unravelling its pathogenesis and developing targeted therapies. In this study, we aimed to investigate tandem repeats in a Chinese cohort of ET pedigrees. To explore the genetic causes of ET, we enrolled 165 Chinese ET pedigrees and performed whole-exome sequencing as well as long-read sequencing within this cohort. Quantitative real-time PCR and western blot analyses were employed to assess HSF1 expression levels. Transgenic Drosophila model and induced pluripotent stem cells (iPSCs) were constructed to investigate the pathogenic role of HSF1 in ET. Our study identified the expanded variable number of tandem repeats (VNTRs) in intron 10 of HSF1. Long-read sequencing revealed two repeat configurations consisting of CCCCGCNCCGCCT and CCNCGCCT in these VNTR loci. Expanded VNTR alleles were highly enriched in ET-affected individuals, and the length of VNTRs was positively correlated with disease severity. We found the intronic repeat expansions downregulated HSF1 expression in affected individuals, indicating its loss-of-function in ET. Consistently, RNAi knockdown of HSF1 homolog in Drosophila led to leg and head shaking and age-dependent movement deficits, recapitulating the ET phenotype in the fly model. iPSCs derived from the ET-affected individual carrying expanded VNTRs in the HSF1 gene exhibited significantly reduced expression of HSF1 compared to control iPSCs. Bulk RNA-sequencing analysis of these iPSCs revealed that diminished HSF1 expression resulted in the downregulation of genes associated with GABAergic synapse function. In conclusion, our study suggests that impaired GABAergic signalling may play a critical role in the pathogenesis of HSF1-related ET. These findings provide new information on the aetiology of ET and highlight the role of HSF1 in human genetic disorders.

Introduction:Parkinson's disease (PD) patients experience a wide variety of gait and posture problems that significantly impair their functional mobility and quality of life. Auditory cue-based training has been shown to improve gait performance in PD patients. However, most of the current methods target gains in bilateral spatiotemporal variables, whereas in the early-stages of PD, symptoms are usually unilateral. Methods:To address the effects of unilateral onset and heterogeneity of early-stage PD on patients' gait performance, we propose a personalized training method based on auditory cues to reduce gait asymmetry between patients' right and left feet. The method targets patients' gait performance through personalized music (auditory cues) and dynamically adjusts the music based on real-time gait data to ensure synchronization with the patient's walking rhythm. Specifically, gait data are acquired in real time via Inertial Measurement Units (IMUs) attached to the ankles of the patient's right and left feet, which are used to calculate the gait cycles of the patient's right and left feet. Personalized music is then generated based on the patient's gait cycle. During the training process, the music is dynamically updated by continuously assessing the synchronization between the patient's gait cycle and the music beats. Results:Fifteen early-stage PD patients(H&Y ≤ 2.5) were initially recruited to compare and analyze the effects of training with and without auditory cues. Gait symmetry improved in all patients who received auditory cues (t = 4.9166, p = 0.0002), with a maximum improvement of 17.685%, and gait variables also showed significant enhancement. Eleven early-stage patients were then recruited for a 7-day intervention, with a mean improvement in gait symmetry of 11.803% (t = 4.391, p = 0.001). There were significant improvements in left-foot velocity (t = 4.613, p = 0.001), right-foot velocity (t = 6.250, p = 0.0001), and right-foot stride length (t = 4.004, p = 0.0025), and the average improvement rate of gait variables reached 37.947%. This indicates that the personalized training method proposed in this paper for the unilateral onset characteristics of early-stage PD is effective. It not only enhances the symmetry of walking in patients with early-stage PD, but also improves motor performance. Discussion:The proposed method can serve as a complementary approach to pharmacological treatment in the rehabilitation of PD patients, demonstrating its effectiveness in clinical application.

BACKGROUND:Parkinson's disease (PD) patients experience gut microbiota dysbiosis. Probiotic intervention could potentially serve as a safe and effective adjunctive therapeutic approach for PD, but its effects on rapid eye movement sleep behavior disorder (RBD) and motor symptoms in PD patients warrant further investigation. OBJECTIVES:To examine the influence of probiotics on RBD, motor symptoms, gut microbiota, and serum metabolites in individuals with PD. METHODS:In this randomized controlled trial, PD patients were randomly allocated to either a probiotics or a control group while maintaining standard treatments. Clinical outcomes, including Unified Parkinson's Disease Rating Scale (UPDRS) and RBD Questionnaire-Hong Kong (RBDQ-HK) were assessed at baseline and post-treatment. Furthermore, fecal and blood samples were collected from PD patients at both timepoints, with additional samples obtained from healthy controls for comparison. The 16S rRNA gene V3-V4 region sequencing method was used to analyze gut microbiota composition, and untargeted metabolomic techniques were utilized to assess serum metabolite alterations, followed by correlation analysis. RESULTS:Fifty eligible PD patients were enrolled and randomly allocated into two groups. After 12 weeks of intervention, the probiotic group showed significant reductions in both UPDRS total scores (-4.8 ± 7.5 vs. 1.8 ± 13.1, p = 0.009) and RBDQ-HK scores (-7.5 ± 6.5 vs. 0 ± 5.8, p = 0.015) compared to controls. Gut microbiota analysis revealed increased abundance of Actinobacteria, Negativicutes, and Bacillus, with reductions in Lactococcus, Comamonas, and Enterococcus after probiotic intervention. Furthermore, compared to normal controls, PD patients exhibited 9 significantly elevated and 11 significantly reduced metabolites; probiotic intervention altered the serum metabolome in PD patients. CONCLUSIONS:This study demonstrated probiotics' potential to ameliorate RBD and motor symptoms while positively affecting the composition of the gut microbiota and serum metabolites in PD patients.

Abstract Background Previous research has commonly regarded overactive bladder (OAB) and restless leg syndrome (RLS) as distinct disorders in terms of their underlying causes, clinical diagnosis, and treatment approaches. However, there is evidence of an overlap in the occurrence of these two conditions following cerebral infarction. Specifically, restless bladder syndrome (RBS), a subtype of RLS, exhibits symptoms similar to those of OAB. Consequently, further investigation is warranted to better understand the relationship between these two disorders. Case presentation In this report, we present the cases of two patients who presented with both OAB following cerebral infarction, along with RLS. Following administration of oral pramipexole, both nocturia and RLS exhibited prompt and efficient alleviation. Conclusions There may exist a shared pathological foundation between certain RLS cases and OAB. In instances where patients exhibit evident OAB symptoms following cerebral infarction and concurrently experience RLS, it is advisable to prioritize the administration of dopaminergic agonists over M receptor inhibitors and β3 agonists. Furthermore, it is plausible that the RBS or a subset of RLS cases could potentially be classified as a form of OAB, although this correlation has yet to be definitively established.

The neurotoxic α-synuclein (α-syn) oligomers play an important role in the occurrence and development of Parkinson’s disease (PD), but the factors affecting α-syn generation and neurotoxicity remain unclear. We here first found that thrombomodulin (TM) significantly decreased in the plasma of PD patients and brains of A53T α-syn mice, and the increased TM in primary neurons reduced α-syn generation by inhibiting transcription factor p-c-jun production through Erk1/2 signaling pathway. Moreover, TM decreased α-syn neurotoxicity by reducing the levels of oxidative stress and inhibiting PAR1-p53-Bax signaling pathway. In contrast, TM downregulation increased the expression and neurotoxicity of α-syn in primary neurons. When TM plasmids were specifically delivered to neurons in the brains of A53T α-syn mice by adeno-associated virus (AAV), TM significantly reduced α-syn expression and deposition, and ameliorated the neuronal apoptosis, oxidative stress, gliosis and motor deficits in the mouse models, whereas TM knockdown exacerbated these neuropathology and motor dysfunction. Our present findings demonstrate that TM plays a neuroprotective role in PD pathology and symptoms, and it could be a novel therapeutic target in efforts to combat PD.

Microstructural alterations in the brain networks of Parkinson’s disease (PD) patients are correlated with gait impairments. Evaluate microstructural alterations in the white matter (WM) fiber bundle tracts using neurite orientation dispersion and density imaging (NODDI) technique in PD versus healthy controls (HC). In this study, 24 PD patients and 29 HC were recruited. NODDI and high-resolution 3D structural images were acquired for each participant. The NODDI indicators, including the intracellular neurite density index (NDI), orientation dispersion index (ODI), and isotropic volume fraction (ISO), were compared between the two groups. Diffusion-weighted (DW) images were preprocessed using MRtrix 3.0 software and the orientation distribution function to trace the main nerve fiber tracts in PD patients. Quantitative gait and clinical assessment scales were used to compare the medication “ON” and “OFF” states of PD patients. The NDI, ODI, and ISO values of the WM fiber bundles were significantly higher in PD patients compared to HC. Fiber bundles, including the anterior thalamic radiation, corticospinal tract, superior longitudinal fasciculus, forceps major, cingulum, and inferior longitudinal fasciculus, were found to be significantly affected in PD. The NDI changes of PD patients were well correlated with stride lengths in the “ON” state; ODI changes were correlated with the stride time in the “ON” and “OFF” states and ISO changes were correlated with the stride time and cadence in the “ON” state. In conclusion, combination of NODDI technique and gait parameters can help detect gait impairment in PD patients early and accurately.

目的:探讨噬血细胞综合征(HLH)患者桥脑病变MRI特征及病因.资料与方法:回顾性分析2019年6月—2022年6月北京友谊医院18例HLH患者桥脑病变的MRI特征及临床资料,MRI分析包括病变位置、平扫及增强信号特征、是否有桥脑外病灶、复查变化,并与临床症状、血液生化结果、脑脊液生化结果进行对照分析.结果:18例患者中16例无中枢神经系统症状;15例(83.3％)病变检出前曾发生电解质紊乱(低钠或低钾),14例行脑脊液检查者3例(21.4％)合并脑脊液生化异常;MRI表现为桥脑中央部病灶,T1WI低信号,T2WI及FLAIR高信号,12例(66.7％)表现为DWI高信号但ADC值不低,3例(16.7％)表现为DWI高信号且ADC值减低,6例(33.3％)检出桥脑外病灶;电解质紊乱纠正及鞘内注射化疗药物后,桥脑病变变化不一,与临床预后无确切关联.结论:当HLH患者发生桥脑中央病变时,可能的原因为桥脑中央髓鞘溶解(CPM)或HLH中枢神经系统(CNS-HLH)受累,临床上需关注电解质变化情况,警惕CPM的发生及进展,同时结合脑脊液生化检查判断有无CNS-HLH并进行针对性的治疗.

Parkinson's disease (PD) is a neurodegenerative disorder with motor deficits due to nigrostriatal dopamine depletion and with the non-motor/premotor symptoms (NMS) such as anxiety, cognitive dysfunction, depression, hyposmia, and sleep disorders. NMS is presented in at least one-fifth of the patients with PD. With the histological information being investigated, stem cells are shown to provide neurotrophic supports and cellular replacement in the damaging brain areas under PD conditions. Pathological change of progressive PD includes degeneration and loss of dopaminergic neurons in the substantia nigra of the midbrain. The current stem cell beneficial effect addresses dopamine boost for the striatal neurons and gliovascular mechanisms as competing for validated PD drug targets. In addition, there are clinical interventions for improving the patient's NMS and targeting their autonomic dysfunction, dementia, mood disorders, or sleep problems. In our and many others' research using brain injury models, multipotent mesenchymal stromal cells demonstrate an additional and unique ability to alleviate depressive-like behaviors, independent of an accelerated motor recovery. Intranasal delivery of the stem cells is discussed for it is extensively tested in rodent animal models of neurological and psychiatric disorders. In this review, we attempt to discuss the repairing potentials of transplanted cells into parkinsonism pathological regions of motor deficits and focus on preventive and treatment effects. From new approaches in the PD biological therapy, it is believed that it can as well benefit patients against PD-NMS.

帕金森病(Parkinson disease,PD)是中老年常见的神经系统退行性疾病,其临床表现主要包括运动症状和非运动症状.快速眼动睡眠行为障碍是PD患者常见的非运动症状,但目前PD伴睡眠行为障碍的发病机制仍然不清楚.近年来研究发现,多模态MRI可能在PD伴睡眠行为障碍的早期诊断、进展及治疗中发挥着重要作用,本文就各类功能MRI技术在PD快速眼动期睡眠行为障碍中的应用作一综述,评估患者脑结构和功能的改变,为临床治疗确立有效的神经影像学标志物.

目的:分析脑淀粉样血管病相关炎症(CAA-ri)患者的临床资料,总结其临床、影像学特征及治疗预后等方面的异质性.方法:选择脑淀粉样血管病相关炎症患者6例,均行头颅核磁检查,其中3例行脑脊液相关检查,2例行APOE基因型检测,2例行病理活检.分析患者的临床资料.结果:该病好发于老年男性,临床异质性包括病程多样性以及症状体征多样性,可为急性、亚急性或慢性病程,亦可为少见的发作性病程;认知障碍、肢体无力、言语障碍和精神行为异常等症状临床出现频次较高.影像学具有共性的不对称白质病变及微出血、含铁血黄素沉积等特征,但病灶范围、程度差异巨大.治疗及转归亦呈高度异质性,激素等免疫相关治疗对重症患者有效,轻症患者可呈自限性病程,但易复发.结论:CAA-ri具有高度临床异质性,但其影像学表现的共性特征可高度提示诊断,激素等治疗有效协助进一步临床确诊.

Introduction: Constipation is one of the common non-motor symptoms in Parkinson's disease that significantly impacts patient quality of life. Probiotics supplementation may improve constipation symptoms, but its effect on the gut microbiota population is unclear.Methods: In this randomized controlled study, 46 PD patients with constipation according to Rome III criteria were recruited. The number of complete bowel movements per week, degree of defecation effort, Bristol stool Scale (BSS), Patient Assessment of Constipation symptom (PAC-SYM) and Patient assessment of constipation quality of life questionnaire (PAC-QOL) were collected pre- and post-intervention to evaluate the constipation symptoms. In addition, fresh feces of subjects before and after intervention and healthy controls were collected for 16s rRNA gene V3-V4 region sequencing to compare bacterial flora differences.Results: Compared with the control group, the treatment group increased the average number of complete bowel movements per week (1.09 +/- 1.24 vs. 0.04 +/- 0.64, P < 0.001). Probiotics supplementation reduced the BSS score (0.65 +/- 0.93 vs. -0.17 +/- 0.94, P = 0.004), PAC-SYM score (4.09 +/- 6.31 vs. -1.83 +/- 4.14, P < 0.001), PAC-QOL score (10.65 +/- 16.53 vs. 0.57 +/- 12.82, P = 0.042), and degree of defecation effort score (1.00 +/- 0.80 vs. 0.00 +/- 0.30, P < 0.001). The improvement rate of constipation in the probiotics group was significantly higher than that in the control group (52.2% vs. 8.7%, P = 0.001). PD patients showed intestinal flora disorders compared to healthy controls. After 12 weeks of probiotics treatment, g_Christensenella_sp._Marseille-P2437 significantly increased, while g_Eubacterium_oxidoreducens_group, g_Eubacterium_hallii_group and s_Odoribacter_sp. _N54.MGS-14 decreased (p < 0 0.05).Conclusions: Probiotics treatment can effectively improve the constipation symptoms of PD patients and positively affected the gut microbiota.