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| 1 | Oxidative stress in Alzheimer's disease显示文摘Oxidative stress plays a significant role in the pathogenesis of Alzheimer's disease(AD), a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons(lipids, proteins, and nucleic acids) can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, infl ammation, and β-amyloid(Aβ) peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment. | Zhichun Chen Chunjiu Zhong | 2014 | Neuroscience Bulletin2014，30，2： | 66 |
| 2 | Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer's Disease显示文摘To date,we still lack disease-modifying therapies for Alzheimer's disease(AD).Here,we report that long-term administration of benfotiamine improved the cognitive ability of patients with AD.Five patients with mild to moderate AD received oral benfotiamine(300 mg daily) over 18 months.All patients were examined by positron emission tomography with Pittsburgh compound B(PiB-PET) and exhibited positive imaging with pamyloid deposition,and three received PiB-PET imaging at follow-up.The five patients exhibited cognitive improvement as assayed by the Mini-Mental Status Examination(MMSE) with an average increase of 3.2 points at month18 of benfotiamine administration.The three patients who received follow-up PiB-PET had a 36.7%increase in the average standardized uptake value ratio in the brain compared with that in the first scan.Importantly,the MMSE scores of these three had an average increase of 3 points during the same period.Benfotiamine significantly improved the cognitive abilities of mild to moderate AD patients independently of brain amyloid accumulation.Our study provides new insight to the development of diseasemodifying therapy. | Xiaoli Pan Zhichun Chen Guoqiang Fei Shumei Pan Weiqi Bao Shuhua Ren Yihui Guan Chunjiu Zhong | 2016 | Neuroscience Bulletin2016，32，6： | 9 |
| 3 | Environmental factors in the development and progression of late-onset Alzheimer's disease显示文摘Late-onset Alzheimer's disease(LOAD) is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarifi ed. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We fi rst discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specifi c pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase–phosphatase imbalance and epigenetic modifi cation at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms. | Moses N. Wainaina Zhichun Chen Chunjiu Zhong | 2014 | Neuroscience Bulletin2014，30，2： | 6 |
| 4 | Complement C7 is a novel risk gene for Alzheimer's disease in Han Chinese显示文摘Alzheimer's disease is the most common neurodegenerative disease,and has a high level of genetic heritability and population heterogeneity.In this study,we performed the whole-exome sequencing of Han Chinese patients with familial and/or early-onset Alzheimer's disease,followed by independent validation,imaging analysis and function characterization.We identified an exome-wide significant rare missense variant rs3792646(p.K420Q)in the C7 gene in the discovery stage(P=1.09×10^(-6),odds ratio=7.853)and confirmed the association in different cohorts and a combined sample(1615 cases and 2832 controls,P_(combined)=2.99×10^(-7),odds ratio=1.930).The risk allele was associated with decreased hippocampal volume and poorer working memory performance in early adulthood,thus resulting in an earlier age of disease onset.Overexpression of the mutant p.K420Q disturbed cell viability,immune activation and β-amyloid processing.Electrophysiological analyses showed that the mutant p.K420Q impairs the inhibitory effect of wild type C7 on the excitatory synaptic transmission in pyramidal neurons.These findings suggested that C7 is a novel risk gene for Alzheimer’s disease in Han Chinese. | Deng-Feng Zhang Yu Fan Min Xu Guihong Wang Dong Wang Jin Li Li-Li Kong Hejiang Zhou Rongcan Luo Rui Bi Yong Wu Guo-Dong Li Ming Li Xiong-Jian Luo Hong-Yan Jiang Liwen Tan Chunjiu Zhong Yiru Fang Chen Zhang Nengyin Sheng Tianzi Jiang Yong-Gang Yao | 2019 | National Science Review2019，6，2： | 6 |
| 5 | Standardized Operational Protocol for Human Brain Banking in China显示文摘With the progress of society, there is an increasing need to tackle disorders of the central nervous system. Human brain tissue, unlike animal tissues, is an irreplaceable resource for the study of neurological diseases (1)Aimed at scientific research and education, the roles of human brain tissue repositories are to acquire brain tissue from donors, prepare, process, and preserve collected samples,provide tissue to specific eligible facilities, and determine the characteristics of each tissue sample. | Wenying Qiu Hanlin Zhang Aimin Bao Keqing Zhu Yue Huang Xiaoxin Yan Jing Zhang Chunjiu Zhong Yong Shen Jiangning Zhou Xiaoying Zheng Liwei Zhang Yousheng Shu Beisha Tang Zhenxin Zhang Gang Wang Ren Zhou Bing Sun Changlin Gong Shumin Duan Chao Ma | 2019 | Neuroscience Bulletin2019，35，2： | 6 |
| 6 | Impaired hippocampal neurogenesis is involved in cognitive dysfunction induced by thiamine deficiency at early pre-pathological lesion stage显示文摘 | Na Zhao Chunjiu Zhong Yang Wang Yanling Zhao Neng Gong Guomin Zhou Tianle Xu Zhen Hong | 2007 | Neurobiology of Disease2007，，2： | 1 |
| 7 | Neuroprotective effects of bone marrow stromal ceils on rat organotypic hippocampal slice culture model of cerebral isechemia显示文摘 | ZHONG Chi QIN Zhen ZHONG Chunjiu | 2003 | Neurosci Lett2003，342，12： | 1 |
| 8 | Brain Energy Improvement as an Emerging Approach for Alzheimer’s Disease Treatment显示文摘Alzheimer’s disease(AD),the most common type of dementia,is a devastating neurodegenerative disorder that seriously afflicts millions of patients and their families due to the lack of effective therapeutic drugs and methods.Elucidating the pathogenesis of this disease has always been a great challenge because AD is complicated with multiple pathophysiological features,including neurodegeneration characterized by progressive synaptic/neuronal loss leading to brain atrophy,brain Aβ deposition forming plaques,Tau hyperphosphorylation constituting neurofibrillary tangles,glial activation and neuroinflammation,and glucose hypometabolism. | Xiaoli Pan Shaoming Sang Chunjiu Zhong | 2021 | Neuroscience Bulletin2021，37，6： | 1 |
| 9 | MR Imaging of Nonalcoholic Wernicke Encephalopathy : A Follow-Up Study 显示文摘 | Chunjiu Zhong Lirong Jin Guoqiang Fei | 2005 | AJNR Am J Neuroradiol2005，26，： | 1 |
| 10 | 显示文摘 | Tang Chunjiu Liu Zugang Zhao Weiming | 1998 | Chinese Journal of Luminescence1998，19，4： | 1 |
| 11 | Correlat ion of thiamine metabolite levels with cognitive function in the non-demented elderly显示文摘Thiamine metabolism is critical for glucose metabolism and also vital for brain function,which is susceptible to decline in the elderly. This study aimed to investigate whether thiamine metabolites correlate with cognitive function in the non-demented elderly and their impact factors. Volunteers >60 years old were recruited and their blood thiamine metabolites and Mini-Mental State Examination(MMSE) scores were measured. The apolipoprotein E(APOE) genotype,routine blood parameters,liver and kidney function,and levels of fasting blood glucose and triglycerides were also measured. The results showed that the thiamine diphosphate(TDP) level weakly correlated with MMSE score in the non-demented elderly. Participants with high TDP levels performed better in Recall and Attention and Calculation than those with low TDP. TDP levels were associated with the APOE ε2 allele,body mass index,hemoglobin level,fasting blood glucose,and triglycerides. Our results suggest that TDP,which is easily affected by many factors,impacts cognitive function in the elderly. | Jingwen Lu Xiaoli Pan Guoqiang Fei Changpeng Wang Lei Zhao Shaoming Sang Huimin Liu Meng Liu Hui Wang Zhiliang Wang Chunjiu Zhong | 2015 | Neuroscience Bulletin2015，31，6： | 1 |
| 12 | Single-nucleotide polymorphisms and haplotypes of non-coding area in the CP gene are correlated with Parkinson's disease显示文摘Our previous studies have demonstrated that ceruloplasmin(CP) dysmetabolism is correlated with Parkinson's disease(PD). However, the causes of decreased serum CP levels in PD patients remain to be clarified. This study aimed to explore the potential association between genetic variants of the CP gene and PD. Clinical features, serum CP levels, and the CP gene(both promoter and coding regions) were analyzed in 60 PD patients and 50 controls. A luciferase reporter system was used to investigate the function of promoter single-nucleotide polymorphisms(SNPs). High-density comparative genomic hybridization microarrays were also used to detect large-scale copy-number variations in CP and an additional 47 genes involved in PD and/or copper/iron metabolism. The frequencies of eight SNPs(one intronic SNP and seven promoter SNPs of the CP gene) and their haplotypes were significantly different between PD patients, especially those with lowered serum CP levels, and controls. However, the luciferase reporter system revealed no significant effect of the risk haplotype on promoter activity of the CP gene. Neither these SNPs nor their haplotypes were correlated with the Hoehn and Yahr staging of PD. The results of this study suggest that common genetic variants of CP are associated with PD and further investigation is needed to explore their functions in PD. | Na Zhao Jianqiu Xiao Zhiyong Zheng Guoqiang Fei Feng Zhang Lirong Jin Chunjiu Zhong | 2015 | Neuroscience Bulletin2015，31，2： | 0 |
| 13 | Physiological Roles of β-amyloid in Regulating Synaptic Function:Implications for AD Pathophysiology显示文摘The physiological functions of endogenous amyloid-β(Aβ),which plays important role in the pathology of Alzheimer's disease(AD),have not been paid enough attention.Here,we review the multiple physiological effects of Aβ,particularly in regulating synaptic transmission,and the possible mechanisms,in order to decipher the real characters of Aβunder both physiological and pathological conditions.Some worthy studies have shown that the deprivation of endogenous Aβgives rise to synaptic dysfunction and cognitive deficiency,while the moderate elevation of this peptide enhances long term potentiation and leads to neuronal hyperexcitability.In this review,we provide a new view for understanding the role of Aβin AD pathophysiology from the perspective of physiological meaning. | Wenwen Cai Linxi Li Shaoming Sang Xiaoli Pan Chunjiu Zhong | 2023 | Neuroscience Bulletin2023，39，8： | 0 |
| 14 | Membrane Aging as the Real Culprit of Alzheimer's Disease:Modification of a Hypothesis显示文摘Our previous studies proposed that Alzheimer's disease(AD) is a metabolic disorder and hypothesized that abnormal brain glucose metabolism inducing multiple pathophysiological cascades contributes to AD pathogenesis. Aging is one of the great significant risk factors for AD. Membrane aging is first prone to affect the function and structure of the brain by impairing glucose metabolism.We presume that risk factors of AD, including genetic factors(e.g., the apolipoprotein E ε4 allele and genetic mutations) and non-genetic factors(such as fat, diabetes,and cardiac failure) accelerate biomembrane aging and lead to the onset and development of the disease. In this review,we further modify our previous hypothesis to demonstrate‘‘membrane aging'' as an initial pathogenic factor that results in functional and structural alterations of membranes and, consequently, glucose hypometabolism and multiple pathophysiological cascades. | Qiujian Yu Chunjiu Zhong | 2018 | Neuroscience Bulletin2018，34，2： | 0 |
| 15 | Protective effect of bone marrow-derived mesenchymal stem cells on dopaminergic neurons against 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in rat brain slices显示文摘BACKGROUND: To date, the use of bone marrow-derived mesenchymal stem cells (MSCs) for the treatment of Parkinson’s disease have solely focused on in vivo animal models. Because of the number of influencing factors, it has been difficult to determine a consistent outcome. OBJECTIVE: To establish an injury model in brain slices of substantia nigra and striatum using 1-methyl-4-phenylpytidinium ion (MPP+), and to investigate the effect of MSCs on dopaminergic neurons following MPP+ induced damage. DESIGN, TIME AND SETTING: An in vitro, randomized, controlled, animal experiment using I mmunohistochemistry was performed at the Laboratory of the Department of Anatomy, Fudan University between January 2004 and December 2006. MATERIALS: Primary MSC cultures were obtained from femurs and tibias of adult Sprague Dawley rats. Organotypic brain slices were isolated from substantia nigra and striatum of 1-day-old Sprague Dawley rat pups. Monoclonal antibodies for tyrosine hydroxylase (TH, 1:5 000) were from Santa Cruz (USA); goat anti-rabbit IgG antibodies labeled with FITC were from Boster Company (China). METHODS: Organotypic brain slices were cultured for 5 days in whole culture medium supplemented with 50% DMEM, 25% equine serum, and 25% Tyrode’s balanced salt solution. The medium was supplemented with 5 μg/mL Ara-C, and the culture was continued for an additional 5 days. The undergrowth of brain slices was discarded at day 10. Eugonic brain slices were cultured with basal media for an additional 7 days. The brain slices were divided into three groups: control, MPP+ exposure, and co-culture. For the MPP+ group, MPP+ (30 μmol/L) was added to the media at day 17 and brain slices were cultured for 4 days, followed by control media. For the co-culture group, the MPP+ injured brain slices were placed over MSCs in the well and were further cultured for 7 days. MAIN OUTCOME MEASURES: After 28 days in culture, neurite outgrowth was examined in the brain slices under phase-contrast microscopy. The percent of area containing dead cells in each brain slice was calculated with the help of propidium iodide fluorescence. Brain slices were stained with antibodies for TH to indicate the presence of dopaminergic neurons. Transmission electron microscopy was applied to determine the effect of MSCs on neuronal ultrastructure. RESULTS: Massive cell death and neurite breakage was observed in the MPP+ group. In addition, TH expression was significantly reduced, compared to the control group (P < 0.01). After 7 days in culture with MSCs, the co-culture group presented with less cell damage and reduced neurite breakage, and TH expression was increased. However, these changes were not significantly different from the MPP+ group (P < 0.01). Electron microscopy revealed reduced ultrastructural injury to cells in the brain slices. However, vacuoles were present in cells, with some autophagic vacuoles. CONCLUSION: Bone marrow-derived MSCs can promote survival of dopaminergic neurons following MPP+-induced neurotoxicity in co-cultures with substantia nigra and striatum brain slices. | Lirong Jin Zhen Hong Chunjiu Zhong Yang Wang | 2009 | Neural Regeneration Research2009，4，1： | 0 |
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