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36 results on '"Pang, Dejiang"'

10. Longitudinal Evolution and Plasma Biomarkers for Excessive Daytime Sleepiness in Parkinson's Disease.

Author

Lin, Junyu, Li, Chunyu, Ou, Ruwei, Hou, Yanbing, Zhang, Lingyu, Wei, Qianqian, Liu, Kuncheng, Jiang, Qirui, Yang, Tianmi, Xiao, Yi, Pang, Dejiang, Yu, Yujiao, Song, Wei, Zhao, Bi, Chen, Xueping, Yang, Jing, Wu, Ying, and Shang, Huifang

Subjects
HYPERSOMNIA, PARKINSON'S disease, GLIAL fibrillary acidic protein, BIOMARKERS, GENERALIZED estimating equations, DROWSINESS
Abstract

Background Excessive daytime sleepiness (EDS) is one of the most frequent nonmotor symptoms in Parkinson's disease (PD); however, the pathogenesis of EDS is unclear, and there is a lack of information on plasma biomarkers for EDS in PD. We aimed to investigate the plasma biomarkers of EDS in a large PD cohort. Methods A total of 159 PD patients were included in the prospective cohort study and followed up annually for 3 years. Plasma biomarkers including glial fibrillary acidic protein, amyloid-beta, p-tau181, and neurofilament light chain (NfL), were measured using an ultrasensitive single-molecule array (Simoa) technology at each visit. EDS was evaluated using the Epworth Sleepiness Scale (ESS). Results The frequency of EDS in PD increased from 15.1% at baseline to 25.0% after 3 years. The mean ESS scores increased from 5.1 (standard deviation [ SD ]: 4.8) at baseline to 6.1 (SD : 5.5) at the third year of follow-up. At baseline, compared with patients with PD without EDS, those with EDS were more likely to be male, had poorer cognitive performance, and more severe motor and nonmotor symptoms. The adjusted generalized estimating equations models showed that higher plasma NfL levels (OR: 1.047 [1.002–1.094], p  = .042) were associated with EDS during follow-ups. The adjusted linear mixed-effects model showed that higher plasma NfL levels (β 0.097 [0.012–0.183], p  = .026) were associated with ESS scores during follow-ups. Conclusions Higher plasma NfL levels were associated with EDS in PD, indicating an association between neuro-axonal degeneration and EDS in PD. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Calcium channel blockers and Parkinson's disease: a systematic review and meta-analysis.

Author

Lin, Junyu, Pang, Dejiang, Li, Chunyu, Ou, Ruwei, Yu, Yujiao, Cui, Yiyuan, Huang, Jingxuan, and Shang, Huifang

Subjects
CALCIUM antagonists, PARKINSON'S disease, NEUROPROTECTIVE agents, DISEASE progression, SYSTEMATIC reviews
Abstract

Background: The calcium channel has been considered to have great potential as a drug target for neuroprotective therapy in Parkinson's disease (PD), but previous studies yielded inconsistent results. Objectives: This study aimed to conduct a systematic review and meta-analysis to assess the relationship between using calcium channel blockers (CCBs) and the risk and progression of PD. Data sources and methods: The terms such as 'Parkinson's disease', 'PD', 'calcium channel blockers', and 'CCB' were used to search the literature published before 1 May 2023 in English databases, including PubMed, Embase, and Cochrane Library, for studies on CCB and PD. Data analysis was performed using Review Manager 5.3 software. Results: A total of 190 works of literature were preliminarily retrieved, and 177 works of literature were excluded by eliminating duplicates, reading abstracts, and reading full texts. A total of nine studies were finally included in the meta-analysis of the CCB and the risk of PD, and five studies were included in the systematic review of the CCB and the progression of PD. A total of 2,961,695 participants were included in the meta-analysis. The random-effects model was used for analysis due to significant heterogeneity. The main results of the meta-analysis showed that the use of CCB could reduce the risk of PD (relative risk 0.78, 95% confidence interval 0.62–0.99). Conclusion: CCB use was associated with a significantly reduced risk of PD. Whether CCB use has a disease-modifying effect on PD needs further study. Registration: PROSPERO: CRD42024508242. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Evolution and Predictive Role of Plasma Alzheimer's Disease-related Pathological Biomarkers in Parkinson's Disease

Author

Lin, Junyu, primary, Ou, Ruwei, additional, Li, Chunyu, additional, Hou, Yanbing, additional, Zhang, Lingyu, additional, Wei, Qianqian, additional, Liu, Kuncheng, additional, Jiang, Qirui, additional, Yang, Tianmi, additional, Xiao, Yi, additional, Pang, Dejiang, additional, Zhao, Bi, additional, Chen, Xueping, additional, Yang, Jing, additional, and Shang, Huifang, additional

Published
2023
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18. Epigenome-Wide Meta-Analysis of Sex-Differential DNA Methylation in Parkinson's Disease

Author

Yang, Tianmi, primary, Li, Chunyu, additional, Wei, Qian-Qian, additional, Pang, Dejiang, additional, Ou, Ru-Wei, additional, Zhang, Lingyu, additional, Cheng, Yang-Fan, additional, Huang, Jingxuan, additional, Lin, Jun-Yu, additional, Che, Ningning, additional, Xiao, Yi, additional, Fu, Jiajia, additional, Jiang, Qirui, additional, Wang, Shichan, additional, Zheng, Xiaoting, additional, Yang, Yongsan, additional, Chen, Yilong, additional, Yu, Haopeng, additional, and Shang, Huifang, additional

Published
2023
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19. Additional file 1 of Shared genetic links between frontotemporal dementia and psychiatric disorders

Author

Li, Chunyu, Pang, Dejiang, Lin, Junyu, Yang, Tianmi, and Shang, Huifang

Subjects
mental disorders, nutritional and metabolic diseases, nervous system diseases
Abstract

Additional file 1: Table S1. Summary data from all GWAS used in current study. Table S2. Risk loci for FTD conditional on psychiatric disorders. Table S3. Shared risk loci between FTD subtypes and psychiatric disorders. Table S4. Risk loci for FTD subtypes conditional on psychiatric disorders. Table S5. eQTL revealing functional effects of shared risk SNPs in human brain tissues. Table S6. Enriched pathways from shared risk genes. Table S7. Enriched gene ontology from shared risk genes. Table S8. Heterogeneity and horizontal pleiotropy analyses between frontotemporal dementia and psychiatric disorders. Figure S1. Genetic correlation between subtypes of FTD and psychiatric diseases. Figure S2. Conditional quantile-quantile plots of nominal versus empirical -log10(P) of each psychiatric disease as a function of significance of association with FTD. Figure S3. Fold-enrichment plots of nominal -log10(P) of psychiatric diseases as a function of significance of association with FTD. Figure S4. Mendelian randomization analysis results between FTD and schizophrenia.

Published
2022
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24. Rheb mediates neuronal-activity-induced mitochondrial energetics through mTORC1-independent PDH activation

Author

Yang, Wanchun, primary, Pang, Dejiang, additional, Chen, Mina, additional, Du, Chongyangzi, additional, Jia, Lanlan, additional, Wang, Luoling, additional, He, Yunling, additional, Jiang, Wanxiang, additional, Luo, Liping, additional, Yu, Zongyan, additional, Mao, Mengqian, additional, Yuan, Qiuyun, additional, Tang, Ping, additional, Xia, Xiaoqiang, additional, Cui, Yiyuan, additional, Jing, Bo, additional, Platero, Alexander, additional, Liu, Yanhui, additional, Wei, Yuquan, additional, Worley, Paul F., additional, and Xiao, Bo, additional

Published
2021
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28. LanCL1 promotes motor neuron survival and extends the lifespan of amyotrophic lateral sclerosis mice

Author

Tan, Honglin, primary, Chen, Mina, additional, Pang, Dejiang, additional, Xia, Xiaoqiang, additional, Du, Chongyangzi, additional, Yang, Wanchun, additional, Cui, Yiyuan, additional, Huang, Chao, additional, Jiang, Wanxiang, additional, Bi, Dandan, additional, Li, Chunyu, additional, Shang, Huifang, additional, Worley, Paul F., additional, and Xiao, Bo, additional

Published
2019
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29. A pectic polysaccharide from water decoction of Xinjiang Lycium barbarum fruit protects against intestinal endoplasmic reticulum stress

Author

Huang, Chao, primary, Yao, Ruyu, additional, Zhu, Zhongkai, additional, Pang, Dejiang, additional, Cao, Xiyue, additional, Feng, Bin, additional, Paulsen, Berit Smestad, additional, Li, Lixia, additional, Yin, Zhongqiong, additional, Chen, Xingfu, additional, Jia, Renrong, additional, Song, Xu, additional, Ye, Gang, additional, Luo, Qihui, additional, Chen, Zhengli, additional, and Zou, Yuanfeng, additional

Published
2019
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33. Developmental and Activity-Dependent Expression of LanCL1 Confers Antioxidant Activity Required for Neuronal Survival

Author

Huang, Chao, primary, Chen, Mina, additional, Pang, Dejiang, additional, Bi, Dandan, additional, Zou, Yi, additional, Xia, Xiaoqiang, additional, Yang, Weiwei, additional, Luo, Liping, additional, Deng, Rongkang, additional, Tan, Honglin, additional, Zhou, Liang, additional, Yu, Shouyang, additional, Guo, Liheng, additional, Du, XiaoXia, additional, Cui, Yiyuan, additional, Hu, Jiahua, additional, Mao, Qing, additional, Worley, Paul F., additional, and Xiao, Bo, additional

Published
2014
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36. Identification of Tmem10 as a novel late-stage oligodendrocytes marker for detecting hypomyelination.

Author

Jiang W, Yang W, Yang W, Zhang J, Pang D, Gan L, Luo L, Fan Y, Liu Y, and Chen M

Subjects
Animals, Base Sequence, Central Nervous System metabolism, Cloning, Molecular, DNA Primers, Mice, Mice, Inbred C57BL, Myelin Proteins genetics, Biomarkers metabolism, Myelin Proteins metabolism, Myelin Sheath metabolism, Oligodendroglia metabolism
Abstract

Oligodendrocytes ensheath axons to form compact insulating multilamellar structures known as myelin. Tmem10 is a novel type I transmembrane glycoprotein that is highly expressed in oligodendrocytes and whose biological function remains largely unknown. Furthermore, the expression pattern of Tmem10 remains a matter of some controversy. Given the inconsistency of its expression pattern and the lack of validated specific antibodies, Tmem10 is not widely accepted as a marker for mature oligodendrocytes. As a means to solve these problems and to aid future studies of oligodendrocyte-associated diseases, we have generated a highly specific Tmem10 antibody. Using this Tmem10 antibody, we clarify that Tmem10 protein is firstly expressed at 2 weeks in the postnatal mouse brain with age-related increase, only in the central nervous system (CNS). We also reveal that Tmem10 is expressed specifically in late stage oligodendrocytes and later than MAG, a late-stage myelin marker. Finally, we show that Tmem10 co-expresses with MOG- and MBP-positive myelin fibers and is dramatically reduced in a hypomyelination mouse model. In conclusion, our study demonstrates that Tmem10 can be used as a specific marker for myelinating oligodendrocytes and perhaps for the evaluation of myelination diseases, such as multiple sclerosis.

Published
2013
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