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| 1 | Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease显示文摘Background:Alzheimer’s disease(AD)is an age-related and progressive neurodegenerative disease that causes substantial public health care burdens.Intensive efforts have been made to find effective and safe treatment against AD.Salidroside(Sal)is the main effective component of Rhodiola rosea L.,which has several pharmacological activities.The objective of this study was to investigate the efficacy of Sal in the treatment of AD transgenic Drosophila and the associated mechanisms.Methods:We used tau transgenic Drosophila line(TAU)in which tau protein is expressed in the central nervous system and eyes by the Gal4/UAS system.After feeding flies with Sal,the lifespan and locomotor activity were recorded.We further examined the appearance of vacuoles in the mushroom body using immunohistochemistry,and detected the levels of total glycogen synthase kinase 3β(t-GSK-3β),phosphorylated GSK-3β(p-GSK-3β),t-tau and p-tau in the brain by western blot analysis.Results:Our results showed that the longevity was improved in salidroside-fed Drosophila groups as well as the locomotor activity.We also observed less vacuoles in the mushroom body,upregulated level of p-GSK-3βand downregulated p-tau following Sal treatment.Conclusion:Our data presented the evidence that Sal was capable of reducing the neurodegeneration in tau transgenic Drosophila and inhibiting neuronal loss.The neuroprotective effects of Sal were associated with its up-regulation of the p-GSK-3βand down-regulation of the p-tau. | Bei Zhang Qiongqiong Li Xingkun Chu Suya Sun Shengdi Chen | 2016 | Translational Neurodegeneration2016，5，1： | 14 |
| 2 | Distinct tissue expression profiles of chicken Lpin1 - α / β isoforms and the effect of the variation on muscle fiber traits显示文摘 | Suya Li Wen Chen Xiangtao Kang Ruili Han Guirong Sun Yanqun Huang | 2012 | Gene2012，，： | 1 |
| 3 | Preparation of Hydrophobic Drugs Cyclodextrin Complex by Lyophilization Monophase Solution显示文摘 | Zhixuan Wang Yingjie Deng Suya Sun Xiaopeng Zhang | 2006 | Drug Development and Industrial Pharmacy2006，，1： | 1 |
| 4 | Paroxetine ameliorates prodromal emotional dysfunction and late-onset memory deficit in Alzheimer’s disease mice显示文摘Background Neuropsychiatric symptoms(NPS)such as depression,anxiety,apathy,and irritability occur in prodromal phases of clinical Alzheimer’s disease(AD),which might be an increased risk for later developing AD.Here we treated young APP/PS1 AD model mice prophylactically with serotonin-selective re-uptake inhibitor(SSRI)paroxetine and investigated the protective role of anti-depressant agent in emotional abnormalities and cognitive defects during disease progress.Methods To investigate the protective role of paroxetine in emotional abnormalities and cognitive defects during disease progress,we performed emotional behaviors of 3 months old APP/PS1 mouse following oral administration of paroxetine prophylactically starting at 1 month of age.Next,we tested the cognitive,biochemical and pathological,effects of long term administration of paroxetine at 6 months old.Results Our results showed that AD mice displayed emotional dysfunction in the early stage.Prophylactic administration of paroxetine ameliorated the initial emotional abnormalities and preserved the eventual memory function in AD mice.Conclusion Our data indicate that prophylactic administration of paroxetine ameliorates the emotional dysfunction and memory deficit in AD mice.These neuroprotective effects are attributable to functional restoration of glutamate receptor(GluN2A)in AD mice. | Peng-Hui Ai Si Chen Xian-Dong Liu Xiao-Na Zhu Yuan-Bo Pan Dong-Fu Feng Shengdi Chen Nan-Jie Xu Suya Sun | 2020 | Translational Neurodegeneration2020，9，2： | 1 |
| 5 | Clinicopathologic characterization and abnormal autophagy of CSF1R-related leukoencephalopathy显示文摘Background:CSF1R-related leukoencephalopathy,also known as hereditary diffuse leukoencephalopathy with spheroids(HDLS),is a rare white-matter encephalopathy characterized by motor and neuropsychiatric symptoms due to colony-stimulating factor 1 receptor(CSF1R)gene mutation.Few of CSF1R mutations have been functionally testified and the pathogenesis remains unknown.Methods:In order to investigate clinical and pathological characteristics of patients with CSF1R-related leukoencephalopathy and explore the potential impact of CSF1R mutations,we analyzed clinical manifestations of 15 patients from 10 unrelated families and performed brain biopsy in 2 cases.Next generation sequencing was conducted for 10 probands to confirm the diagnosis.Sanger sequencing,segregation analysis and phenotypic reevaluation were utilized to substantiate findings.Functional examination of identified mutations was further explored.Results:Clinical and neuroimaging characteristics were summarized.The average age at onset was 35.9±6.4 years(range 24–46 years old).Younger age of onset was observed in female than male(34.2 vs.39.2 years).The most common initial symptoms were speech dysfunction,cognitive decline and parkinsonian symptoms.One patient also had marked peripheral neuropathy.Brain biopsy of two cases showed typical pathological changes,including myelin loss,axonal spheroids,phosphorylated neurofilament and activated macrophages.Electron microscopy disclosed increased mitochondrial vacuolation and disorganized neurofilaments in ballooned axons.A total of 7 pathogenic variants(4 novel,3 documented)were identified with autophosphorylation deficiency,among which c.2342C>T remained partial function of autophosphorylation.Western blotting disclosed the significantly lower level of c.2026C>T(p.R676*)than wild type.The level of microtubule associated protein 1 light chain 3-II(LC3-II),a classical marker of autophagy,was significantly lower in mutants expressed cells than wild type group by western blotting and immunofluorescence staining.Conclusions:Our findings support the loss-of-function and haploinsufficiency hypothesis in pathogenesis.Autophagy abnormality may play a role in the disease.Repairing or promoting the phosphorylation level of mutant CSF1R may shed light on therapeutic targets in the future.However,whether peripheral polyneuropathy potentially belongs to CSF1R-related spectrum deserves further study with longer follow-up and more patients enrolled. | Wo-Tu Tian Fei-Xia Zhan Qing Liu Xing-Hua Luan Chao Zhang Liang Shang Ben-Yan Zhang Si-Jian Pan Fei Miao Jiong Hu Ping Zhong Shi-Hua Liu Ze-Yu Zhu Hai-Yan Zhou Suya Sun Xiao-Li Liu Xiao-Jun Huang Jing-Wen Jiang Jian-Fang Ma Ying Wang Shu-Fen Chen Hui-Dong Tang Sheng-Di Chen Li Cao | 2019 | Translational Neurodegeneration2019，8，1： | 0 |
| 6 | Targeting neuroplasticity in neurodegenerative diseases stimulation techniques显示文摘Deficits in synaptic transmission and plasticity are thought to contribute to the pathophysiology of Alzheimer's disease(AD)and Parkinson's disease(PD).Several brain stimulation techniques are currently available to assess or modulate human neuroplasticity,which could offer clinically useful interventions as well as quantitative diagnostic and prognostic biomarkers.In this review,we discuss several brain stimulation techniques,with a special emphasis on transcranial magnetic stimulation and deep brain stimulation(DBS),and review the results of clinical studies that applied these techniques to examine or modulate impaired neuroplasticity at the local and network levels in patients with AD or PD.The impaired neuroplasticity can be detected in patients at the earlier and later stages of both neurodegenerative diseases.However,current brain stimulation techniques,with a notable exception of DBS for PD treatment,cannot serve as adequate clinical tools to assist in the diagnosis,treatment,or prognosis of individual patients with AD or PD.Targeting the impaired neuroplasticity with improved brain stimulation techniques could offer a powerful novel approach for the treatment of AD and PD. | Ti-Fei Yuan Wei-Guang Li Chencheng Zhang Hongjiang Wei Suya Sun Nan-Jie Xu Jun Liu Tian-Le Xu | 2020 | Translational Neurodegeneration2020，9，4： | 0 |
| 7 | Covalent-architected molybdenum disulfide arrays on Ti_(3)C_(2)T_(x) MXene fiber towards robust capacitive energy storage显示文摘Ti_(3)C_(2)T_(x)MXene fiber has shown extraordinary potential for supercapacitor electrode in wearable elec-tronics and textile energy storage,but realizing high energy density and practical-powered applications remains a great challenge.Here,we report a covalent-architected molybdenum disulfide-Ti_(3)C_(2)T_(x)(MoS_(2)-Ti_(3)C_(2)T_(x))core-shell fiber for high-performance supercapacitor.Benefiting from the microfluidic and micro-reaction strategies,the ordered MoS_(2)arrays are strongly bridged on Ti_(3)C_(2)T_(x)fiber via Ti-O-Mo bond,re-sulting in large exposed surface,enhanced porosity and excellent interfacial conduction for charges high diffusion and faradaic transfer.The MoS_(2)-Ti_(3)C_(2)T_(x)fiber exhibits ultra-large capacitance of 2028 F cm^(-3)and admirable reversibility in 1 M H_(2)SO_(4)aqueous electrolyte.Meanwhile,MoS_(2)-Ti_(3)C_(2)T_(x)fiber-based solid-state supercapacitor presents high energy density of 23.86 mWh cm^(-3),capacitance of 1073.6 F cm^(-3)and superior cycling ability of 92.13%retention after 20,000 cycles,which can realize stable energy supply for wearable watch,LEDs,electric fans,toy ship and self-powered devices.Our work may provide an insight-ful guidance for the advanced design of structural fiber towards robust new energy and next-generation wearable industry. | Suya Sun Xiaolin Zhu Xingjiang Wu Meigui Xu Ying Hu Ningzhong Bao Guan Wu | 2023 | Journal of Materials Science & Technology2023，，8： | 0 |
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