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Article: Alpha-Synuclein Accumulation and Its Phosphorylation in the Enteric Nervous System of Patients Without Neurodegeneration: An Explorative Study.

Bu, Lu-Lu / Huang, Kai-Xun / Zheng, De-Zhi / Lin, Dan-Yu / Chen, Ying / Jing, Xiu-Na / Liang, Yan-Ran / Tao, En-Xiang

2020 Volume 12, Page(s) 575481

Abstract: Alpha-synuclein (α-Syn) is widely distributed and involved in the regulation of the nervous system. The phosphorylation of α-Syn at serine 129 ( ... ...

Abstract	Alpha-synuclein (α-Syn) is widely distributed and involved in the regulation of the nervous system. The phosphorylation of α-Syn at serine 129 (p
Language	English
Publishing date	2020-11-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2020.575481
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Article: LncRNA-T199678 Mitigates α-Synuclein-Induced Dopaminergic Neuron Injury via miR-101-3p.

Bu, Lu-Lu / Xie, Ying-Yu / Lin, Dan-Yu / Chen, Ying / Jing, Xiu-Na / Liang, Yan-Ran / Peng, Su-Dan / Huang, Kai-Xun / Tao, En-Xiang

Frontiers in aging neuroscience

2020 Volume 12, Page(s) 599246

Abstract: Parkinson's disease (PD) is the second most common neurodegenerative disorder characterized by dopaminergic neuron death and the abnormal accumulation and aggregation of α-synuclein (α-Syn) in the substantia nigra (SN). Although the abnormal accumulation ...

Abstract	Parkinson's disease (PD) is the second most common neurodegenerative disorder characterized by dopaminergic neuron death and the abnormal accumulation and aggregation of α-synuclein (α-Syn) in the substantia nigra (SN). Although the abnormal accumulation of α-Syn can solely promote and accelerate the progress of PD, the underlying molecular mechanisms remain unknown. Mounting evidence confirms that the abnormal expression of long non-coding RNA (lncRNA) plays an important role in PD. Our previous study found that exogenous α-Syn induced the downregulation of lncRNA-T199678 in SH-SY5Y cells via a gene microarray analysis. This finding suggested that lncRNA-T199678 might have a potential pathological role in the pathogenesis of PD. This study aimed to explore the influence of lncRNA-T199678 on α-Syn-induced dopaminergic neuron injury. Overexpression of lncRNA-T199678 ameliorated the neuron injury induced by α-Syn via regulating oxidative stress, cell cycle, and apoptosis. Studies indicate lncRNAs could regulate posttranscriptional gene expression via regulating the downstream microRNA (miRNA). To discover the downstream molecular target of lncRNA-T199678, the following experiment found out that miR-101-3p was a potential target for lncRNA-T199678. Further study showed that the upregulation of lncRNA-T199678 reduced α-Syn-induced neuronal damage through miR-101-3p in SH-SY5Y cells and lncRNA-T199678 was responsible for the α-Syn-induced intracellular oxidative stress, dysfunction of the cell cycle, and apoptosis. All in all, lncRNA-T199678 mitigated the α-Syn-induced dopaminergic neuron injury via targeting miR-101-3p, which contributed to promote PD. Our results highlighted the role of lncRNA-T199678 in mitigating dopaminergic neuron injury in PD and revealed a new molecular target for PD.
Language	English
Publishing date	2020-11-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2020.599246
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Article ; Online: Design, synthesis and identification of N, N-dibenzylcinnamamide (DBC) derivatives as novel ligands for α-synuclein fibrils by SPR evaluation system.

Chen, Yan-Fei / Bian, Jiang / Zhang, Peng / Bu, Lu-Lu / Shen, Yan / Yu, Wen-Bo / Lu, Xiu-Hong / Lin, Xin / Ye, De-Yong / Wang, Jian / Chu, Yong

Bioorganic & medicinal chemistry

2020 Volume 28, Issue 7, Page(s) 115358

Abstract: PET imaging of α-synuclein (α-syn) deposition in the brain will be an effective tool for earlier diagnosis of Parkinson's disease (PD) due to α-syn aggregation is the widely accepted biomarker for PD. However, the necessary PET radiotracer for imaging is ...

Abstract	PET imaging of α-synuclein (α-syn) deposition in the brain will be an effective tool for earlier diagnosis of Parkinson's disease (PD) due to α-syn aggregation is the widely accepted biomarker for PD. However, the necessary PET radiotracer for imaging is clinically unavailable until now. The lead compound discovery is the first key step for the study. Herein, we initially established an efficient biologically evaluation system well in highthroughput based on SPR technology, and identified a novel class of N, N-dibenzylcinnamamide (DBC) compounds as α-syn ligands through the assay. These compounds were proved to have high affinities against α-syn aggregates (K
MeSH term(s)	Brain ; Cinnamates/chemistry ; Cinnamates/pharmacology ; Drug Design ; Humans ; Ligands ; Molecular Structure ; Positron-Emission Tomography ; Radioligand Assay ; alpha-Synuclein/chemistry
Chemical Substances	Cinnamates ; Ligands ; alpha-Synuclein
Language	English
Publishing date	2020-02-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1161284-8
ISSN	1464-3391 ; 0968-0896
ISSN (online)	1464-3391
ISSN	0968-0896
DOI	10.1016/j.bmc.2020.115358
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Zs.A 3815: Show issues

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Article ; Online: Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy.

Bu, Lu-Lu / Liu, Yi-Qi / Shen, Yan / Fan, Yun / Yu, Wen-Bo / Jiang, Dong-Lang / Tang, Yi-Lin / Yang, Yu-Jie / Wu, Ping / Zuo, Chuan-Tao / Koprich, James B / Liu, Feng-Tao / Wu, Jian-Jun / Wang, Jian

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2021 Volume 18, Issue 2, Page(s) 962–978

Abstract: Glucagon-like peptide-1 (GLP-1) receptor stimulation ameliorates parkinsonian motor and non-motor deficits in both experimental animals and patients; however, the disease-modifying mechanisms of GLP-1 receptor activation have remained unknown. The ... ...

Abstract	Glucagon-like peptide-1 (GLP-1) receptor stimulation ameliorates parkinsonian motor and non-motor deficits in both experimental animals and patients; however, the disease-modifying mechanisms of GLP-1 receptor activation have remained unknown. The present study investigated whether exendin-4 (a GLP-1 analogue) can rescue motor deficits and exert disease-modifying effects in a parkinsonian rat model of α-synucleinopathy. This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections. Positron emission tomography/computed tomography (PET/CT) scanning and immunostaining established that treatment with exendin-4 attenuated tyrosine-hydroxylase-positive neuronal loss and terminal denervation and mitigated the decrease in expression of vesicular monoamine transporter 2 within the nigrostriatal dopaminergic systems of rats injected with AAV-9-A53T-α-synuclein. It also mitigated the parkinsonian motor deficits assessed in behavioral tests. Furthermore, through both in vivo and in vitro models of Parkinson's disease, we showed that exendin-4 promoted autophagy and mediated degradation of pathological α-synuclein, the effects of which were counteracted by 3-methyladenine or chloroquine, the autophagic inhibitors. Additionally, exendin-4 attenuated dysregulation of the PI3K/Akt/mTOR pathway in rats injected with AAV-9-A53T-α-synuclein. Taken together, our results demonstrate that exendin-4 treatment relieved behavioral deficits, dopaminergic degeneration, and pathological α-synuclein aggregation in a parkinsonian rat model of α-synucleinopathy and that these effects were mediated by enhanced autophagy via inhibiting the PI3K/Akt/mTOR pathway. In light of the safety and tolerance of exendin-4 administration, our results suggest that exendin-4 may represent a promising disease-modifying treatment for Parkinson's disease.
MeSH term(s)	Animals ; Autophagy/drug effects ; Autophagy/physiology ; Cell Line, Tumor ; Exenatide/pharmacology ; Exenatide/therapeutic use ; Female ; Humans ; Neuroprotection/drug effects ; Neuroprotection/physiology ; Parkinsonian Disorders/chemically induced ; Parkinsonian Disorders/pathology ; Parkinsonian Disorders/prevention & control ; Rats ; Rats, Sprague-Dawley ; Synucleinopathies/chemically induced ; Synucleinopathies/pathology ; Synucleinopathies/prevention & control ; alpha-Synuclein/toxicity
Chemical Substances	alpha-Synuclein ; Exenatide (9P1872D4OL)
Language	English
Publishing date	2021-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-021-01018-5
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Zs.A 6156: Show issues

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Article ; Online: Fasudil Promotes α-Synuclein Clearance in an AAV-Mediated α-Synuclein Rat Model of Parkinson's Disease by Autophagy Activation.

Yang, Yu-Jie / Bu, Lu-Lu / Shen, Cong / Ge, Jing-Jie / He, Shu-Jin / Yu, Hui-Ling / Tang, Yi-Lin / Jue, Zhao / Sun, Yi-Min / Yu, Wen-Bo / Zuo, Chuan-Tao / Wu, Jian-Jun / Wang, Jian / Liu, Feng-Tao

Journal of Parkinson's disease

2020 Volume 10, Issue 3, Page(s) 969–979

Abstract: Background: Parkinson's disease (PD) is the second most common neurodegenerative disorder, but the disease-modifying therapies focusing on the core pathological changes are still unavailable. Rho-associated protein kinase (ROCK) has been suggested as a ... ...

Abstract	Background: Parkinson's disease (PD) is the second most common neurodegenerative disorder, but the disease-modifying therapies focusing on the core pathological changes are still unavailable. Rho-associated protein kinase (ROCK) has been suggested as a promising target for developing neuroprotective therapies in PD. Objective: We aimed to explore the promotion of α-synuclein (α-syn) clearance in a rat model. Methods: In a rat model induced by unilateral injection of adeno-associated virus of serotype 9 (AAV9) expressing A53T α-syn (AAV9-A53T-α-syn) into the right substantia nigra, we aimed to investigate whether Fasudil could promote α-syn clearance and thereby attenuate motor impairments and dopaminergic deficits. Results: In our study, treatment with Fasudil (5 mg/kg rat weight/day) for 8 weeks significantly improved the motor deficits in the Cylinder and Rotarod tests. In the in vivo positron emission tomography imaging with the ligand 18F-dihydrotetrabenazine, Fasudil significantly enhanced the dopaminergic imaging in the injected striatum of the rat model (p < 0.05 vs. vehicle group, p < 0.01 vs. left striatum in Fasudil group). The following mechanistic study confirmed that Fasudil could promote the autophagic clearance of α-syn by Becline 1 and Akt/mTOR pathways. Conclusion: Our study suggested that Fasudil, the ROCK2 inhibitor, could attenuate the anatomical and behavioral lesions in the Parkinsonian rat model by autophagy activation. Our results identify Fasudil as a drug with high translational potential as disease-modifying treatment for PD and other synucleinopathies.
MeSH term(s)	Animals ; Autophagy/physiology ; Disease Models, Animal ; Dopamine/metabolism ; Dopaminergic Neurons/metabolism ; Female ; Neurodegenerative Diseases/metabolism ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Rats, Sprague-Dawley ; Substantia Nigra/metabolism ; Substantia Nigra/pathology ; alpha-Synuclein/metabolism
Chemical Substances	Snca protein, rat ; alpha-Synuclein ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2020-06-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2620609-2
ISSN	1877-718X ; 1877-7171
ISSN (online)	1877-718X
ISSN	1877-7171
DOI	10.3233/JPD-191909
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Zs.A 6964: Show issues

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Article: Toward precision medicine in Parkinson's disease.

Bu, Lu-Lu / Yang, Ke / Xiong, Wei-Xi / Liu, Feng-Tao / Anderson, Boyd / Wang, Ye / Wang, Jian

Annals of translational medicine

2016 Volume 4, Issue 2, Page(s) 26

Abstract: Precision medicine refers to an innovative approach selected for disease prevention and health promotion according to the individual characteristics of each patient. The goal of precision medicine is to formulate prevention and treatment strategies based ...

Abstract	Precision medicine refers to an innovative approach selected for disease prevention and health promotion according to the individual characteristics of each patient. The goal of precision medicine is to formulate prevention and treatment strategies based on each individual with novel physiological and pathological insights into a certain disease. A multidimensional data-driven approach is about to upgrade "precision medicine" to a higher level of greater individualization in healthcare, a shift towards the treatment of individual patients rather than treating a certain disease including Parkinson's disease (PD). As one of the most common neurodegenerative diseases, PD is a lifelong chronic disease with clinical and pathophysiologic complexity, currently it is treatable but neither preventable nor curable. At its advanced stage, PD is associated with devastating chronic complications including both motor dysfunction and non-motor symptoms which impose an immense burden on the life quality of patients. Advances in computational approaches provide opportunity to establish the patient's personalized disease data at the multidimensional levels, which finally meeting the need for the current concept of precision medicine via achieving the minimal side effects and maximal benefits individually. Hence, in this review, we focus on highlighting the perspectives of precision medicine in PD based on multi-dimensional information about OMICS, molecular imaging, deep brain stimulation (DBS) and wearable sensors. Precision medicine in PD is expected to integrate the best evidence-based knowledge to individualize optimal management in future health care for those with PD.
Language	English
Publishing date	2016-01-28
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.3978/j.issn.2305-5839.2016.01.21
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Article ; Online: Cdk5-Dependent Activation of Neuronal Inflammasomes in Parkinson's Disease.

Zhang, Pei / Shao, Xiao-Yun / Qi, Guang-Jian / Chen, Qiang / Bu, Lu-Lu / Chen, Li-Jun / Shi, Jing / Ming, Jie / Tian, Bo

Movement disorders : official journal of the Movement Disorder Society

2016 Volume 31, Issue 3, Page(s) 366–376

Abstract: Background: Inflammasomes, which mediate the activation of caspase-1 and maturation of IL-1β and IL-18, have been unambiguously verified to participate in many diseases, such as lung diseases, infectious diseases and Alzheimer's disease, but the ... ...

Abstract	Background: Inflammasomes, which mediate the activation of caspase-1 and maturation of IL-1β and IL-18, have been unambiguously verified to participate in many diseases, such as lung diseases, infectious diseases and Alzheimer's disease, but the relation between Parkinson's disease and inflammasomes is poorly understood. Methods: The expression, maturation, and secretion of inflammasomes in neurons were measured. The activation of inflammasomes in the substantia nigra of the brain was tested in acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and an α-synuclein transgenic mouse model. The levels of IL-1β and IL-18 in cerebrospinal fluid and serum samples of Parkinson's disease (PD) patients and control subjects were measured. The role of cyclin-dependent kinase 5 (Cdk5) in neuronal inflammasome activation was evaluated using the pharmacological Cdk5 inhibitor roscovitine or Cdk5-targeted deletion. Results: Here, we observed the expression of core molecules of inflammasomes, including NALP3, ASC, caspase-1, and IL-1β, in neuronal cells. The PD inducer rotenone could activate neuronal inflammasomes and promote the maturation and secretion of the cleaved IL-1β and IL-18 in a dose- and time-dependent manner. We also detected the activation of inflammasomes in the substantia nigra of a PD mouse model and in cerebrospinal fluid of PD patients. Furthermore, Cdk5 is required for the activation of inflammasomes, and both inhibition and deletion of Cdk5 could efficiently block inflammasome activation in PD models. Conclusions: Together, our results indicated that Cdk5-dependent activation of neuronal inflammasomes was involved in the progression of PD.
MeSH term(s)	Animals ; Cyclin-Dependent Kinase 5/metabolism ; Disease Models, Animal ; Inflammasomes/metabolism ; Mice ; Mice, Inbred C57BL ; Neurons/metabolism ; Parkinson Disease/metabolism ; Substantia Nigra/metabolism
Chemical Substances	Inflammasomes ; Cyclin-Dependent Kinase 5 (EC 2.7.11.1) ; Cdk5 protein, mouse (EC 2.7.11.22)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.26488
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Zs.A 2555: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Depressive Symptoms Are Associated With Color Vision but not Olfactory Function in Patients With Parkinson's Disease.

Li, Da-Ke / Liu, Feng-Tao / Chen, Kui / Bu, Lu-Lu / Yang, Ke / Chen, Chen / Liu, Zhen-Yang / Tang, Yi-Lin / Zhao, Jue / Sun, Yi-Min / Wang, Jian / Wu, Jian-Jun

The Journal of neuropsychiatry and clinical neurosciences

2018 Volume 30, Issue 2, Page(s) 122–129

Abstract: Depressive symptoms and sensory dysfunction, such as reduction in visual and olfactory function, are common in Parkinson's disease (PD). Previous studies have suggested that depressive symptoms are associated with visual impairments and potentially with ... ...

Abstract	Depressive symptoms and sensory dysfunction, such as reduction in visual and olfactory function, are common in Parkinson's disease (PD). Previous studies have suggested that depressive symptoms are associated with visual impairments and potentially with hyposmia in several types of mood disorders. However, the relationship between depressive symptoms and sensory dysfunction remains unclear in PD. To examine the association of depressive symptoms with color vision and olfactory function in PD, the authors conducted a cross-sectional study in 159 patients with PD. Depressive symptoms were measured with the Beck Depression Inventory-II (BDI-II) and the 30-item Geriatric Depression Scale (GDS-30); color vision was tested with the Farnsworth-Munsell 100 Hue Test (FMT); and olfactory function was tested with the Sniffin' Sticks Screening 12 Test. Results showed that the total error score (TES) for the FMT was significantly and independently correlated with scores on both the BDI-II and GDS-30 in a positive manner, suggesting that more severe depressive symptoms are associated with poorer color vision in PD. In addition, both somatic and effective subscores for the BDI-II were correlated with the TES on the FMT, while no significant correlation was observed between total scores on the Sniffin' Sticks Screening 12 Test and BDI-II or GDS-30. The decrease in color vision but not olfactory function was found to be associated with the severity of depressive symptoms in PD patients, supporting the idea that the occurrence of depressive symptoms in PD is linked with disruption of the visual system.
MeSH term(s)	Aged ; Color Vision ; Cross-Sectional Studies ; Depression/physiopathology ; Female ; Humans ; Male ; Middle Aged ; Parkinson Disease/physiopathology ; Psychiatric Status Rating Scales ; Smell
Language	English
Publishing date	2018-02-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1036340-3
ISSN	1545-7222 ; 0895-0172
ISSN (online)	1545-7222
ISSN	0895-0172
DOI	10.1176/appi.neurospych.17030063
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Zs.A 2633: Show issues

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Article ; Online: Autophagic Modulation by Trehalose Reduces Accumulation of TDP-43 in a Cell Model of Amyotrophic Lateral Sclerosis via TFEB Activation.

Wang, Ying / Liu, Feng-Tao / Wang, Yi-Xuan / Guan, Rong-Yuan / Chen, Chen / Li, Da-Ke / Bu, Lu-Lu / Song, Jie / Yang, Yu-Jie / Dong, Yi / Chen, Yan / Wang, Jian

Neurotoxicity research

2018 Volume 34, Issue 1, Page(s) 109–120

Abstract: Amyotrophic lateral sclerosis (ALS) is the most common adult-onset motor neuron disease characterized by the formation of protein inclusion and progressive loss of motor neurons, finally leading to muscle weakness and respiratory failure. So far, the ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is the most common adult-onset motor neuron disease characterized by the formation of protein inclusion and progressive loss of motor neurons, finally leading to muscle weakness and respiratory failure. So far, the effective drugs for ALS are yet to be developed. Impairment of transcriptional activator transcription factor EB (TFEB) has been demonstrated as a key element in the pathogenesis of ALS. Trehalose is an mechanistic target of rapamycin-independent inducer for autophagy, which showed autophagic activation and neuroprotective effect in a variety of neurodegenerative diseases. The mechanism for trehalose-induced autophagy enhancement is not clear, and its therapeutic effect on TAR DNA-binding protein-43 (TDP-43) proteinopathies has been poorly investigated. Here we examined the effect of trehalose on TDP-43 clearance in a cell culture model and identified that trehalose treatment significantly reduced TDP-43 accumulation in vitro through modulation of the autophagic degradation pathway. Further studies revealed that activation of TFEB induced by trehalose was responsible for the enhancement of autophagy and clearance of TDP-43 level. These results gave us the notion that TFEB is a central regular in trehalose-mediated autophagic clearance of TDP-43 aggregates, representing an important step forward in the treatment of TDP-43 related ALS diseases.
MeSH term(s)	Animals ; Autophagy/drug effects ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Glucose/pharmacology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Neuroblastoma/pathology ; Time Factors ; Transfection ; Trehalose/therapeutic use
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DNA-Binding Proteins ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; TARDBP protein, human ; TFEB protein, human ; Green Fluorescent Proteins (147336-22-9) ; Trehalose (B8WCK70T7I) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/s12640-018-9865-7
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Article ; Online: Evaluation of PDQ-8 and its relationship with PDQ-39 in China: a three-year longitudinal study.

Chen, Kui / Yang, Yu-Jie / Liu, Feng-Tao / Li, Da-Ke / Bu, Lu-Lu / Yang, Ke / Wang, Ying / Shen, Bo / Guan, Rong-Yuan / Song, Jie / Wang, Jian / Wu, Jian-Jun

Health and quality of life outcomes

2017 Volume 15, Issue 1, Page(s) 170

Abstract: Background: Parkinson's disease is characterized by motor and non-motor symptoms with wide ranging impacts on the health-related quality of life. The 39-item Parkinson's disease Questionnaire (PDQ-39) is the most widely used PD-specific health-related ... ...

Abstract	Background: Parkinson's disease is characterized by motor and non-motor symptoms with wide ranging impacts on the health-related quality of life. The 39-item Parkinson's disease Questionnaire (PDQ-39) is the most widely used PD-specific health-related quality-of-life questionnaire. The short-form 8-item Parkinson's disease Questionnaire (PDQ-8) was found to produce results similar to that of the PDQ-39 cross-culturally. However, there is no evaluation of the PDQ-8 in the mainland of China. Methods: In this longitudinal study, 283 patients with Parkinson's disease were recruited. The PDQ-39, the PDQ-8 and other scales were administered. Patients attended the clinic once annually for three years to complete the scales. Results: The PDQ-8 was found to have good validity and reliability. There was a strong correlation between the summary indices of the PDQ-8 and the PDQ-39 (r=0.93, P<0.001). Results suggested that the PDQ-8 was also associated with other clinical scales of mobility, depression and cognition. The convergent validity and discriminant validity of the PDQ-8 were demonstrated by item-to-dimension correlations. There was acceptable internal consistency of the PDQ-8 (Cronbach's α: 0.80; Item-scale correlation efficient: 0.56-0.72). The PDQ-8 replicated the results of the PDQ-39 well at all follow-up time points (intraclass correlation coefficient: 0.96-0.98). In addition, there was good test-retest reliability of the PDQ-8. Conclusion: The PDQ-8 is a valid and reliable instrument assessing health-related quality of life for PD patients in the mainland of China.
Language	English
Publishing date	2017-08-24
Publishing country	England
Document type	Journal Article
ISSN	1477-7525
ISSN (online)	1477-7525
DOI	10.1186/s12955-017-0742-5
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