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Neural Regeneration Research 2015年第2期10卷 205-207页

作者： Rubina Marzagalli Alessandro Castorina department of Biomedical Sciences and Biotechnologies Section of Human Anatomy and Histology University of Catania

Alzheimer＇s disease （AD） is the most common neurodegenerative disorder, and its incidence is relatively high among elderly people, affecting about 1-2% of the population between 60-65 years old and rising dramatically （about 30%） in people aged 80 years or older （Selkoe, 2002）. Nowadays, considering the increasing mean lifespan of populations in developed countries, the disease is becoming more and more a health concern, and the search for an effective cure has turned into＂a real need＂.

关键词： The seeming paradox of adenosine receptors as targets for the treatment of Alzheimer’s disease agonists or antagonists

Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity

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Neural Regeneration Research 2014年第4期9卷 385-393页

作者： Lihong Zhou Hui Wang Jia Luo Kun Xiong Leping Zeng Dan Chen Jufang Huang department of human anatomy and Neurobiology School of Basic Medical ScienceCentral South University

Various retinal injuries induced by ocular hypertension have been shown to induce plastic changes in retinal synapses, but the potential regulatory mechanism of synaptic plasticity after retinal injury was still unclear. A rat model of acute ocular hypertension was established by injecting saline intravitreally for an hour, and elevating the intraocular pressure to 14.63 kPa （110 mmHg）. Western blot assay and immunofluorescence results showed that synaptophysin expression had a distinct spatiotemporal change that increased in the inner plexiform layer within 1 day and spread across the outer plexiform layer after 3 days. Glial fibrillary acidic protein expression in retinae was greatly increased after 3 days, and reached a peak at 7 days, which was also consistent with the peak time of synaptophysin expression in the outer plexiform layer following the increased intraocular pressure. Fluorocitrate, a glial metabolic inhibitor, was intravitreally injected to inhibit glial cell activation following high intraocular pressure. This significantly inhibited the enhanced glial fibrillary acidic protein expression induced by high intraocular pressure injury. Synaptophysin expression also decreased in the inner plexiform layer within a day and the widened distribution in the outer plexiform layer had disappeared by 3 days. The results suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin.

关键词： nerve regeneration neuronal plasticity retina synapses synaptophysin glial cells highintraocular pressure fluorocitrate glial fibrillary acidic protein NSFC grant neural regeneration

Potential significance of CX3CR1 dynamics in stress resilience against neuronal disorders

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Neural Regeneration Research 2022年第10期17卷 2153-2156页

作者： Koichi Inoue department of Integrative anatomy Nagoya City University Graduate School of Medical SciencesNagoyaJapan

Recent findings have implicated inflammatory responses in the central nervous system in a variety of neuropsychiatric and neurodegenerative diseases,and the understanding and control of immunological responses could be a major factor of future therapeutic strategies for neurological ***,derived from myelogenous cells,respond to a number of stimuli and make immune responses,resulting in a prominent role as cells that act on inflammation in the central nervous ***(FKN or CX3CL1)signaling is an important factor that influences the inflammatory response of *** receptor for FKN,CX3CR1,is usually expressed in microglia in the brain,and therefore the inflammatory response of microglia is modified by ***,FKN often suppresses inflammatory responses in microglia and activation of its receptor may be effective in the treatment of inflammatory neurological ***,it has also been suggested that inflammatory responses facilitated by FKN signaling aggravate neurological ***,further studies are still required to resolve the conflicting interpretation of the protective or deleterious contribution of microglial FKN *** notably,regulation of FKN signaling has recently been shown to be beneficial in the treatment of human diseases,although not neurological *** addition,a CX3CR1 inhibitor has been developed and successfully tested in animal models,and it is expected to be in human clinical trials in the *** this review,I describe the potential therapeutic consideration of microglial CX3CR1 dynamics through altered FKN signaling.

关键词： Alzheimer’s disease CX3CR1 fractalkine inflammation knockout mice microglia resilience SARS-CoV-2 stress stroke

TIGAR promotes neural stem cell differentiation through acetyl-CoA-mediated histone acetylation

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TIGAR promotes neural stem cell differentiation through acet...

Intellectual disability-related chromatin regulator Brpf1 affects electrophysiological feature of hippocampal neurons and related pathways

中国解剖学会2019年年会

作者： Wenjuan Zhou Tiantian Zhao Jingyi Du Guangyu Ji Xinyue Li Shufang Ji Wenyu Tian Xu Wang Aijun Hao department of human anatomy and histoembryology School of Basic Medical ScienceShandong University

＜正＞The metabolic transition from aerobic glycolysis to oxidative phosphorylation has been regarded as a hallmark of neuronal *** what triggers metabolism reprogramming and how glucose metabolism directs neural stem...

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Intellectual disability-related chromatin regulator Brpf1 af...

Lipid rafts participate in aberrant degradative autophagic-lysosomal pathway of amyloid-beta peptide in Alzheimer's disease

中国解剖学会2021年年会

作者： Xian Weiwei Yuan Xiangshan Cao Jingli Zhou Guomin You Linya department of human anatomy & histoembryology School of Basic Medical SciencesFudan University

Intellectual disability (ID) is a prevalent neurodevelopmental disorder,affecting 1%-2%of *** researches revealed that haploinsufficiency of Brpfl could result in *** plays important roles in learning and memory which are impaired in people with *** study the roles of Brpf1 in hippocampus, we investigated the morphology,electrophysiology and molecular mechanism in both cultured mouse hippocampal neurons by infecting with AAV-shBrpfl virus and in mouse model by injecting into hippocampal CA1 area with AAV-shBrpfl virus.

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Neural Regeneration Research 2014年第1期9卷 92-100页

作者： Xin Zhou Chun Yang Yufeng Liu Peng Li Huiying Yang Jingxing Dai Rongmei Qu Lin Yuan department of human anatomy Histology and EmbryologySchool of Basic Medical SciencesSouthern Medical University

Amyloid-beta peptide is the main component of amyloid plaques, which are found in Alzhei- mer＇s disease. The generation and deposition of amyloid-beta is one of the crucial factors for the onset and progression of Alzheimer＇s disease. Lipid rafts are glycolipid-rich liquid domains of the plasma membrane, where certain types of protein tend to aggregate and intercalate. Lipid rafts are involved in the generation of amyloid-beta oligomers and the formation of amyloid-beta peptides. In this paper, we review the mechanism by which lipid rafts disturb the aberrant deg- radative autophagic-lysosomal pathway of amyloid-beta, which plays an important role in the pathological process of Alzheimer＇s disease. Moreover, we describe this mechanism from the view of the Two-system Theory of fasciology and thus, suggest that lipid rafts may be a new target of Alzheimer＇s disease treatment.

关键词： nerve regeneration lipid rafts amyloid precursor protein autophagy lysosome Alzhei-mer's disease Two-system Theory amyloid beta peptide autophagosome National Financial MajorProject of China neural regeneration

The effects and mechanisms of TOX3 and TIGAR on the proliferation and differentiation of neural stem cells

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The effects and mechanisms of TOX3 and TIGAR on the prolifer...

Mesenchymal stem cells-based therapy as a potential treatment in neurodegenerative disorders: is the escape from senescence an answer?

中国解剖学会2021年年会

作者： Zhou Wenjuan Zhao Tiantian Du Jingyi Ji Guangyu Wu Dong Zhao Man Hao Aijun department of human anatomy and histoembryology School of Basic Medical ScienceShandong University

The formation of cerebral cortex is a highly ordered and strictly regulated development process,involving the production of various neural cells and the formation of nerve *** proliferation,differentiation,migration and stratification of NSCs are the cytological basis of cerebral cortex *** is important to understand the potential molecular mechanism of proliferation and differentiation of NSCs.

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Neural Regeneration Research 2015年第6期10卷 850-858页

作者： Alessandro Castorina Marta Anna Szychlinska Rubina Marzagalli Giuseppe Musumeci department of Biomedical and Biotechnological Science Section of Human Anatomy and HistologySchool of MedicineUniversity of Catania

Aging is the most prominent risk factor contributing to the development of neurodegenerative disorders. In the United States, over 35 million of elderly people suffer from age-related diseases. Aging impairs the self-repair ability of neuronal cells, which undergo progressive deterioration. Once initiated, this process hampers the already limited regenerative power of the central nervous system, making the search for new therapeutic strategies particularly difficult in elderly affected patients. So far, mesenchymal stem cells have proven to be a viable option to ameliorate certain aspects of neurodegeneration, as they possess high proliferative rate and differentiate in vitro into multiple lineages. However, accumulating data have demonstrated that during longterm culture, mesenchymal stem cells undergo spontaneous transformation. Transformed mesenchymal stem cells show typical features of senescence, including the progressive shortening of telomers, which results in cell loss and, as a consequence, hampered regenerative potential. These evidences, in line with those observed in mesenchymal stem cells isolated from old donors, suggest that senescence may represent a limit to mesenchymal stem cells exploitation in therapy, prompting scholars to either find alternative sources of pluripotent cells or to arrest the age-re- lated transformation. In the present review, we summarize findings from recent literature, and critically discuss some of the major hurdles encountered in the search of appropriate sources of mesenchymal stem cells, as well as benefits arising from their use in neurodegenerative diseases. Finally, we provide some insights that may aid in the development of strategies to arrest or, at least, delay the aging of mesenchymal stem cells to improve their therapeutic potential.

关键词： aging neurodegenerative disorders telomere shortening MSCs cellular therapy

Effects of sericin on heme oxygenase-1 expression in the hippocampus and cerebral cortex of type 2 diabetes mellitus rats

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Neural Regeneration Research 2011年第6期6卷 423-427页

作者： Zhihong Chen Yaqiang He Wenliang Fu Jingfeng Xue department of human anatomy Chengde Medical University Chengde 067000 Hebei Province China

Previous studies have demonstrated that sericin effectively reduces blood glucose, and protects islet cells, as well as the gonads and kidneys. However, whether sericin improves diabetes mellitus-induced structural and functional problems in the central nervous system remains poorly understood. Rat models of type 2 diabetes mellitus were established by intraperitoneal injection of streptozotocin. The present study observed histological changes in the hippocampus and cerebral cortex, as well as heme oxygenase-1 expression, and explored sericin effects on the central nervous system in diabetic rats. Pathological damage to neural cells in the rat hippocampus and cerebral cortex was relieved following intragastric administration of sericin at a dose of 2.4 g/kg for 35 consecutive days. Heme oxygenase-1 protein and mRNA expressions were decreased in the hippocampus and cerebral cortex of diabetes mellitus rats after sericin treatment. The results suggest that sericin plays a protective effect on the nervous system by decreasing the high expression of heme oxygenase-1 following diabetes mellitus.

关键词： sericin diabetes mellitus hippocampus cerebral cortex heme oxygenase-1

Next generation drug connectivity mapping for acquiring therapeutic agents to differentially regulate myelination

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Neural Regeneration Research 2023年第4期18卷 797-798页

作者： Kasum Azim Andrea Domenico Rivera Arthur Morgan Butt department of Neurology Medical FacultyHeinrich-Heine-UniversityDüsseldorfGermany Institute of Biomedical and Biomolecular Sciences School of Pharmacy and Biomedical ScienceUniversity of PortsmouthSt Michael’s BuildingWhite Swan RoadPortsmouthUK Section of human anatomy Department of NeuroscienceUniversity of PaduaPaduaItaly

The need for new therapeutic approaches:Conventional drug discovery is a lengthy and expensive process,taking decades and billions of dollars to get a drug from bench to *** of the costs incurred are at the pre-clinical stages,between drug design and synthesis to delineating the cellular“Mechanisms of Action”(MoA).Notably,there is a very high risk of failure,and only a very small proportion of therapeutic agents reach later-phase clinical ***,drug repositioning has become a valuable strategy aimed at fast-tracking treatments into clinical use and improving the chances of therapeutic success.A novel addition to this approach is connectivity mapping,which defines cell-specific transcriptional responses to small molecules in disease-dependent *** commentary outlines how some of the latest innovations in connectivity mapping can be exploited for drug repurposing.

关键词： connectivity dollar therapeutic