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| 1 | The recommendations of Chinese Parkinson’s disease and movement disorder society consensus on therapeutic management of Parkinson’s disease显示文摘Background:Parkinson’s disease(PD)is a chronic,progressive and debilitating disease,which affects over 2.5 million people in China.PD is characterized clinically by resting tremor,muscular rigidity,bradykinesia and postural instability.As the disease progresses,additional complications can arise such as non-motor and neurobehavioral symptoms.Pharmacological treatment and surgical intervention for PD have been implemented in China.Until 10 years ago,there was lack of standardization for the management of PD in different regions and among different physicians,leading to different treatment levels in different regions and different physicians.Since then,the Chinese Parkinson’s Disease and Movement Disorder Society have published three versions of guidelines for the management of PD in China,in 2006,2009 and 2014,respectively.Correspondingly,the overall level of treatment for PD in China improved.Objectives:To update the treatment guidelines based on current foreign and domestic practice guidelines and clinical evidence,and to improve the treatment options available to physicians in the management of PD.Summary:A variety of treatment recommendations in the treatment guidelines have been proposed,including physical activity and disease-modifying medication,which should be initiated at the early-stage of the disease.The principles of dosage titration should be followed to avoid acute adverse reactions to the drugs,to achieve a satisfactory clinical effect with a low dose and to reduce the incidence of long-term motor complications.Moreover,different treatment strategies should be considered at different stages of the disease.Importantly,treatment guidelines and personalized treatments should be valued equally.A set of treatment recommendations has been developed to assist physicians to improve and optimize clinical outcomes for patients with PD in China. | Shengdi Chen Piu Chan Shenggang Sun Haibo Chen Baorong Zhang Weidong Le Chunfeng Liu Guoguang Peng Beisha Tang Lijuan Wang Yan Cheng Ming Shao Zhenguo Liu Zhenfu Wang Xiaochun Chen Mingwei Wang Xinhua Wan Huifang Shang Yiming Liu Pingyi Xu Jian Wang Tao Feng Xianwen Chen Xingyue Hu Anmu Xie Qin Xiao | 2016 | Translational Neurodegeneration2016，5，1： | 23 |
| 2 | Role of autophagy in the pathogenesis of multiple sclerosis显示文摘Autophagy plays an important role in maintaining the cellular homeostasis. One of its functions is to degrade unnecessary organelles and proteins for energy recycling or amino-acids for cell survival. Ablation of autophagy leads to neurodegeneration. Multiple sclerosis(MS), a permanent neurological impairment typical of chronic inflammatory demyelinating disorder, is an auto-immune disease of the central nervous system(CNS). Autophagy is tightly linked to the innate and adaptive immune systems during the autoimmune process, and several studies have shown that autophagy directly participates in the progress of MS or experimental autoimmune encephalomyelitis(EAE, a mouse model of MS). Dysfunction of mitochondria that intensively influences the autophagy pathway is one of the important factors in the pathogenesis of MS. Autophagy-related gene(ATG) 5 and immune-related GTPase M(IRGM) 1 are increased, while ATG16L2 is decreased, in T-cells in EAE and active relapsing-remitting MS brains. Administration of rapamycin, an inhibitor of mammalian target of rapamycin( m TOR), ameliorates relapsing-remitting EAE. Inflammation and oxidative stress are increased in MS lesions and EAE, but Lamp2 and the LC3-II/LC3-I ratio are decreased. Furthermore, autophagy in various glial cells plays important roles in regulating neuro-inflammation in the CNS, implying potential roles in MS. In this review, we discuss the role of autophagy in the peripheral immune system and the CNS in neuroinflammation associated with the pathogenesis of MS. | Peizhou Liang Weidong Le | 2015 | Neuroscience Bulletin2015，31，4： | 19 |
| 3 | Molecular network of neuronal autophagy in the pathophysiology and treatment of depression显示文摘Major depressive disorder(MDD) is a complicated multifactorial induced disease, characterized by depressed mood, anhedonia, fatigue, and altered cognitive function. Recently, many studies have shown that antidepressants regulate autophagy. In fact, autophagy, a conserved lysosomal degradation pathway, is essential for the central nervous system. Dysregulation of autophagic pathways, such as the mammalian target of rapamycin(m TOR) signaling pathway and the beclin pathway, has been studied in neurodegenerative diseases. However, autophagy in MDD has not been fully studied. Here, we discuss whether the dysregulation of autophagy contributes to the pathophysiology and treatment of MDD and summarize the current evidence that shows the involvement of autophagy in MDD. | Jack Jia Weidong Le | 2015 | Neuroscience Bulletin2015，31，4： | 12 |
| 4 | Biomarkers for Parkinson’s Disease: How Good Are They?显示文摘Parkinson’s disease(PD)is a complex neurodegenerative disorder with no cure in sight.Clinical challenges of the disease include the inability to make a definitive diagnosis at the early stages and difficulties in predicting the disease progression.The unmet demand to identify reliable biomarkers for early diagnosis and management of the disease course of PD has attracted a lot of attention.However,only a few reported candidate biomarkers have been tried in clinical practice at the present time.Studies on PD biomarkers have often overemphasized the discovery of novel identity,whereas efforts to further evaluate such candidates are rare.Therefore,we update the new development of biomarker discovery in PD and discuss the standard process in the evaluation and assessment of the diagnostic or prognostic value of the identified potential PD biomarkers in this review article.Recent developments in combined biomarkers and the current status of clinical trials of biomarkers as outcome measures are also discussed.We believe that the combination of different biomarkers might enhance the specificity and sensitivity over a single measure that might not be sufficient for such a multiplex disease. | Tianbai Li Weidong Le | 2020 | Neuroscience Bulletin2020，36，2： | 12 |
| 5 | Histone deacetylase 6 delays motor neuron degeneration by ameliorating the autophagic flux defect in a transgenic mouse model of amyotrophic lateral sclerosis显示文摘Amyotrophic lateral sclerosis(ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons. Abnormal protein aggregation and impaired protein degradation are believed to contribute to the pathogenesis of this disease. Our previous studies showed that an autophagic flux defect is involved in motor neuron degeneration in the SOD1G93 A mouse model of ALS. Histone deacetylase 6(HDAC6) is a class II deacetylase that promotes autophagy by inducing the fusion of autophagosomes to lysosomes. In the present study, we showed that HDAC6 expression was decreased at the onset of disease and became extremely low at the late stage in ALS mice. Using lentivirus-HDAC6 gene injection, we found that HDAC6 overexpression prolonged the lifespan and delayed the motor neuron degeneration in ALS mice. Moreover, HDAC6 induced the formation of autolysosomes and accelerated the degradation of SOD1 protein aggregates in the motor neurons of ALS mice. Collectively, our results indicate that HDAC6 has neuroprotective effects in an animal model of ALS by improving the autophagic flux in motor neurons, and autophagosome-lysosome fusion might be a therapeutic target for ALS. | Sheng Chen Xiao-Jie Zhang Li-Xi Li Yin Wang Ru-Jia Zhong Weidong Le | 2015 | Neuroscience Bulletin2015，31，4： | 9 |
| 6 | Cellulose synthesis genes CESA6 and CSI1 are important for salt stress tolerance in Arabidopsis显示文摘Soil salinity is a widespread abiotic stress constraint threatening agricultural production,as it severely inhibits growth and development of crops.Several salt stress signaling pathways have been discovered in the model plant Arabidopsis thaliana,which include components for sensing the stress,transmitting the signal and regulating the downstream genes(Deinlein et al.2014;Julkowska | Shuang-Shuang Zhang Le Sun Xinran Dong Sun-Jie Lu Weidong Tian Jian-Xiang Liu | 2016 | Journal of Integrative Plant Biology2016，58，7： | 9 |
| 7 | Autophagy is involved in oral rAAV/Aβ vaccine-induced Aβ clearance in APP/PS1 transgenic mice显示文摘The imbalance between β-amyloid(Aβ) generation and clearance plays a fundamental role in the pathogenesis of Alzheimer 's disease(AD). The sporadic form of AD is characterized by an overall impairment in Aβ clearance. Immunotherapy targeting Aβ clearance is believed to be a promising approach and is under active clinical investigation. Autophagy is a conserved pathway for degrading abnormal protein aggregates and is crucial for Aβ clearance. We previously reported that oral vaccination with a recombinant AAV/Aβ vaccine increased the clearance of Aβ from the brain and improved cognitive ability in AD animal models, while the underlying mechanisms were not well understood. In this study, we first demonstrated that oral vaccination with rAAV/Aβ decreased the p62 level and up-regulated the LC3BII/LC3B-I ratio in APP/PS1 mouse brain, suggesting enhanced autophagy. Further, inhibition of the Akt/m TOR pathway may account for autophagy enhancement. We also found increased anti-Aβ antibodies in the sera of APP/PS1 mice with oralvaccination, accompanied by elevation of complement factors C1 q and C3 levels in the brain. Our results indicate that autophagy is closely involved in oral vaccination-induced Aβ clearance, and modulating the autophagy pathway may be an important strategy for AD prevention and intervention. | He-Cheng Wang Tao Zhang Bolati Kuerban Ying-Lan Jin Weidong Le Hideo Hara Dong-Sheng Fan Yan-Jiang Wang Takeshi Tabira De-Hua Chui | 2015 | Neuroscience Bulletin2015，31，4： | 8 |
| 8 | Dynamic changes of CX3CL1/CX3CR1 axis during microglial activation and motor neuron loss in the spinal cord of ALS mouse model显示文摘Background:Neuron-microglia communication plays a crucial role in the motor neurons(MNs)death in amyotrophic lateral sclerosis(ALS).Neurons can express chemokine(C-X3-C motif)ligand 1(CX3CL1),which mediates microglial activation via interacting with its sole receptor CX3CR1 in microglia.In the present study,we aimed to investigate the dynamic changes of CX3CL1/CX3CR1 axis during microglial activation and MNs loss in SOD1G93A mouse model of ALS.Methods:qPCR,western blot and immunofluorescent staining were used to examine the mRNA and protein levels and localization of CX3CL1/CX3CR1 in the anterior horn region of spinal cord in both SOD1G93A mice and their agematched wild type(WT)littermates at 40,60,90 and 120 days of age.The M1/M2 microglial activation in the spinal cord tissues of SOD1G93A mice and WT mice were evaluated by immunofluorescent staining of M1/M2 markers and further confirmed by qPCR analysis of M1/M2-related cytokines.Results:The immunofluorescent staining revealed that CX3CL1 was predominately expressed in MNs,while CX3CR1 was highly expressed in microglia in the anterior horn region of spinal cord.Compared with age-matched WT mice,CX3CL1 mRNA level was elevated at 40 days but decreased at 90 and 120 days in the anterior horn region of spinal cords in ALS mice.Consistently,CX3CR1 mRNA level was increased at 90 and 120 days.Western blot assay further confirmed the dynamic changes of CX3CL1/CX3CR1 axis in ALS mice.Additionally,the levels of M1/M2 markers of microglia and their related cytokines in the anterior horn region of spinal cord in ALS mice were increased at 90 and 120 days.Moreover,while M1-related cytokines in ALS mice were persistently increased at 120 days,the upregulated M2-related cytokines started to decline at 120 days,suggesting an altered microglial activation.Conclusions:Our data revealed the dynamic changes of CX3CL1/CX3CR1 axis and an imbalanced M1/M2 microglial activation during ALS pathological progression.These findings may help identify potential molecular targets for ALS therapy. | Jingjing Zhang Yufei Liu Xinyao Liu Song Li Cheng Cheng Sheng Chen Weidong Le | 2018 | Translational Neurodegeneration2018，7，1： | 7 |
| 9 | Hyposmia: a possible biomarker of Parkinson's disease显示文摘Hyposmia, identified as reduced sensitivity to odor, is a common non-motor symptom of Parkinson’s disease (PD) that antedates the typical motor symptoms by several years. It occurs in ~90% of early-stage cases of PD. In addition to the high prevalence, the occurrence of hyposmia may also predict a higher risk of PD. Investigations into hyposmia and its relationship with PD may help elucidate the underlying pathogenic mechanisms. This review provides an update of olfactory dysfunction in PD and its potential as a biomarker for this devastating disease. | Qian Xiao Sheng Chen Weidong Le | 2014 | Neuroscience Bulletin2014，30，1： | 7 |
| 10 | Tiny But Mighty:Promising Roles of MicroRNAs in the Diagnosis and Treatment of Parkinson's Disease显示文摘Parkinson's disease(PD) is the second most common age-related neurodegenerative disorder after Alzheimer's disease. To date, the clinical diagnosis of PD is primarily based on the late onset of motor impairments. Unfortunately, at this stage, most of the dopaminergic neurons may have already been lost, leading to the limited clinical benefits of current therapeutics.Therefore, early identification of PD, especially at the prodromal stage, is still a main challenge in the diagnosis and management of this disease. Recently, microRNAs(miRNAs) in cerebrospinal fluid or peripheral blood have been proposed as putative biomarkers to assist in PD diagnosis and therapy. In this review, we systematically summarize the changes of miRNA expression profiles in PD patients, and highlight their putative roles in the diagnosis and treatment of this devastating disease. | Ying Wang Zhaofei Yang Weidong Le | 2017 | Neuroscience Bulletin2017，33，5： | 6 |
| 11 | Biomarker Discovery in Parkinson's Disease:Present Challenges and Future Opportunities显示文摘Parkinson's disease(PD)is the second most common neurodegenerative disorder affecting more than 1%of the older population.Histopathologically,PD is characterized by a severe loss of dopaminergic neurons in the substantia nigra and cytoplasmic inclusions composed of insoluble protein aggregates(Lewy bodies),which lead to a progressive movement disorder including the classic triad of tremor,bradykinesia,and rigidity. | Song Li Weidong Le | 2017 | Neuroscience Bulletin2017，33，5： | 5 |
| 12 | Milestones of Parkinson's Disease Research:200 Years of History and Beyond显示文摘Parkinson's disease(PD)is the second most common neurodegenerative disease worldwide.Since its first description as a neurological disorder by James Parkinson(1755–1824)in 1817,many important discoveries have been made during this 200 years of PD research history.These milestones have revealed many aspects of PD,including clinical and pathological characteristics。 | Song Li Weidong Le | 2017 | Neuroscience Bulletin2017，33，5： | 5 |
| 13 | Selective role of autophagy in neuronal function and neurodegenerative diseases显示文摘Proteostasis is critical for neuronal maintenance and survival,and its imbalance leads to neurodegeneration with the hallmark of protein misfolding and aggregation[1].Macroautophagy becomes a major route for the clearance of protein aggregates that are normally poor substrates for the proteasome,the other protein quality-control machinery[2].As a flux process。 | Yan-Ning Rui Weidong Le | 2015 | Neuroscience Bulletin2015，31，4： | 4 |
| 14 | Recent Progress in Non-motor Features of Parkinson’s Disease with a Focus on Circadian Rhythm Dysregulation显示文摘Parkinson’s disease(PD)is the second most common neurodegenerative disease,which manifests with both motor and non-motor symptoms.Circadian rhythm dysregulation,as one of the most challenging non-motor features of PD,usually appears long before obvious motor symptoms.Moreover,the dysregulated circadian rhythm has recently been reported to play pivotal roles in PD pathogenesis,and it has emerged as a hot topic in PD research.In this review,we briefly introduce the circadian rhythm and circadian rhythm-related genes,and then summarize recent research progress on the altered circadian rhythm in PD,ranging from clinical features to the possible causes of PD-related circadian disorders.We believe that future comprehensive studies on the topic may not only help us to explore the mechanisms of PD,but also shed light on the better management of PD. | Yufei Liu Long Niu Xinyao Liu Cheng Cheng Weidong Le | 2021 | Neuroscience Bulletin2021，37，7： | 4 |
| 15 | Enhancement of fine particle filtration with efficient humidification显示文摘Filtration is one of the most effective methods to remove suspended fine particles from air. In filtration processes,pressure drop of compact dust cake causes problems in efficiency and economy, which has received increasing attention and still remains challenging. In this study, we developed a novel technique to intensify the filtration of fine particles with efficient humidification. Two strategies for humidification, including ultrasonic atomization and steam humidification(controlling of ambient humidity), were employed and proved to be both effective. The regeneration frequency of the filter could be reduced by 55% with ultrasonic atomization, while steam humidification could lead to a 78% reduction in regeneration frequency. The effect of operating conditions on pressure drop and the mass loading during filtration were investigated. The dust cake showed a loose and porous structure with an optimized droplet-to-particle ratio. With the ratio of 1.53 and 0.0282, the maximum mass loading was 552 g·m-2upon the ultrasonic atomization and 720 g·m-2upon the steam humidification. The results show that humidification could slow down the increase of pressure drop during filtration and improve the efficiency of process. | Yumei Zhang Weidong Zhang Zhengyu Yang Junteng Liu Fushen Yang Ning Li Le Du | 2016 | Chinese Journal of Chemical Engineering2016，24，4： | 3 |
| 16 | Altered Motor Performance,Sleep EEG,and Parkinson’s Disease Pathology Induced by Chronic Sleep Deprivation in Lrrk2^(G2019S) Mice显示文摘Parkinson’s disease(PD)is a multifaceted disease in which environmental variables combined with genetic predisposition cause dopaminergic(DAergic)neuron loss in the substantia nigra pars compacta.The mutation of leucine-rich repeat kinase 2(Lrrk2)is the most common autosomal dominant mutation in PD,and it has also been reported in sporadic cases.A growing body of research suggests that circadian rhythm disruption,particularly sleep-wake abnormality,is common during the early phase of PD.Our present study aimed to evaluate the impact of sleep deprivation(SD)on motor ability,sleep performance,and PD pathologies in Lrrk2^(G2019S) transgenic mice.After two months of SD,Lrrk2^(G2019S) mice at 12 months of age showed an exacerbated PD-like phenotype with motor deficits,a reduced striatal DA level,degenerated DAergic neurons,and altered sleep structure and biological rhythm accompanied by the decreased protein expression level of circadian locomotor output cycles kaput Lrrk2 gene in the brain.All these changes persisted and were even more evident in 18-month-old mice after 6 months of follow-up.Moreover,a significant increase inα-synuclein aggregation was found in SD-treated transgenic mice at 18 months of age.Taken together,our findings indicate that sleep abnormalities,as a risk factor,may contribute to the pathogenesis and progression of PD.Early detection of sleep disorders and improvement of sleep quality may help to delay disease progression and provide long-term clinical benefits. | Xinyao Liu Hang Yu Yuanyuan Wang Song Li Cheng Cheng Murad Al-Nusaif Weidong Le | 2022 | Neuroscience Bulletin2022，38，10： | 3 |
| 17 | Association of ABCB1 Gene Polymorphisms with Efficacy and Adverse Reaction to Risperidone or Paliperidone in Han Chinese Schizophrenic Patients显示文摘Dear editor,P-glycoprotein(P-gp,also known as ATP-binding cassette transport sub-family B member 1,ABCB1)is a potent ATP-dependent efflux pump for a wide variety of drugs.Although studies of its substrates are abundant[1,2],and ABCB1 is a well-conserved gene,there is increasing evidence that its polymorphisms affect substrate specificity[3].A previous study reported that the synonymous | Weifeng Mi Feihu Liu Yongqiao Liu Bo Du Weidong Xiao Lingzhi Li Lan Huang Tianlan Lu Jia He Le Shi Weihua Yue Hongyan Zhang | 2016 | Neuroscience Bulletin2016，32，6： | 3 |
| 18 | Can Biomarkers Help the Early Diagnosis of Parkinson's Disease?显示文摘Parkinson's disease(PD) is a complex neurodegenerative disease with progressive loss of dopamine neurons. PD patients usually manifest a series of motor and non-motor symptoms. In order to provide better early diagnosis and subsequent disease-modifying therapies for PD patients, there is an urgent need to identify sensitive and specific biomarkers. Biomarkers can be divided into four categories: clinical, imaging, biochemical, and genetic. Ideal biomarkers not only improve our understanding of PD pathogenesis and progression, but also provide benefits for early risk evaluation and clinical diagnosis of PD. Although many efforts have been made and several biomarkers have been extensively investigated,few if any have been found useful for early diagnosis.Here, we summarize recent developments in the discoveredbiomarkers of PD and discuss their merits and limitations for the early diagnosis of PD. | Weidong Le Jie Dong Song Li Amos D. Korczyn | 2017 | Neuroscience Bulletin2017，33，5： | 2 |
| 19 | Hot Topics in Recent Parkinson’s Disease Research:Where We are and Where We Should Go显示文摘Parkinson’s disease(PD),the second most common neurodegenerative disease,is clinically characterized by both motor and non-motor symptoms.Although overall great achievements have been made in elucidating the etiology and pathogenesis of PD,the exact mechanisms of this complicated systemic disease are still far from being clearly understood.Consequently,most of the currentlyused diagnostic tools and therapeutic options for PD are symptomatic.In this perspective review,we highlight the hot topics in recent PD research for both clinicians and researchers.Some of these hot topics,such as sleep disorders and gut symptoms,have been neglected but are currently emphasized due to their close association with PD.Following these research directions in future PD research may help understand the nature of the disease and facilitate the discovery of new strategies for the diagnosis and therapy of PD. | Song Li Congcong Jia Tianbai Li Weidong Le | 2021 | Neuroscience Bulletin2021，37，12： | 2 |
| 20 | NLRP3 Inflammasome-Mediated Neuroinflammation and Related Mitochondrial Impairment in Parkinson's显示文摘Parkinson's disease(PD)is a common neuro-degenerative disorder caused by the loss of dopamine neu-rons in the substantia nigra and the formation of Lewy bod-ies,which are mainly composed of alpha-synuclein fibrils.Alpha-synuclein plays a vital role in the neuroinflamma-tion mediated by the nucleotide-binding oligomerization domain-,leucine-rich repeat-,and pyrin domain-containing protein 3(NLRP3)inflammasome in PD.A better under-standing of the NLRP3 inflammasome-mediated neuroin-flammation and the related mitochondrial impairment during PD progression may facilitate the development of promis-ing therapies for PD.This review focuses on the molecular mechanisms underlying NLRP3 inflammasome activation,comprising priming and protein complex assembly,as well as the role of mitochondrial impairment and its subsequent inflammatory effects on the progression of neurodegenera-tion in PD.In addition,the therapeutic strategies targeting the NLRP3 inflammasome for PD treatment are discussed,including the inhibitors of NLRP3 inflammatory pathways,mitochondria-focused treatments,microRNAs,and other therapeutic compounds. | Qiu-Qin Han Weidong Le | 2023 | Neuroscience Bulletin2023，39，5： | 2 |
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