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Journal of Biosciences and Medicines 2023年第11期11卷 65-75页

作者： Zhenying Yu Hongyan Wu Department of endocrine The First Affiliated Hospital of Yangtze University Jingzhou China

In recent years, the incidence of neurodegenerative diseases, mainly Alzheimer’s disease, Parkinson’s disease, vascular dementia, and cerebral ischemia, has been rising gradually, which has a serious impact on the physiological state and quality of life of human beings in old age, and the current clinical drugs are unsatisfactory in terms of therapeutic efficacy and healing, which has made this kind of diseases become a social medical problem. Tea polyphenols are the main functional components of tea and have great potential in neuroprotection. In this paper, we review the research on tea polyphenols in neurodegenerative diseases, with the aim of providing a new entry point for the treatment of neurodegenerative diseases.

关键词： neurodegenerative diseases Tea Polyphenols Neuroprotection

Vitamin E in ataxia and neurodegenerative diseases:A review

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World Journal of Neuroscience 2012年第4期2卷 217-222页

作者： Fatima Imounan Naima Bouslam Jehanne Aasfara Kaoutar El Alaoui Wafa Regragui El Hachmia Ait Benhaddou Ahmed Bouhouche Ali Benomar Mohamed Yahyaoui Mohammed V Souissi University CHU Ibn SinaNeurology B and Neurogenetics DepartmentHopital des SpecialitesRabatMorocco Mohammed V Souissi University Faculte de Medecine et de Pharmacie RabatCentre de Recherche en Epidemiologie Clinique et Essais Therapeutiques(CRECET)RabatMorocco

Vitamin E is one of the most important lipid-soluble antioxidants. It is essential for the neurological function but its role in the central nervous system has not fully been elucidated. It is known that tocopherol acts in protecting cell membranes from oxidative damage and it can act as an anti-in?ammatory agent, which may also be neuroprotective, as well as regulating speci?c enzymes. There is growing evidence that oxidative stress plays a key role in the pathophysiology of several neurodegenerative disorders. These diseases are defined by the progressive loss of speci?c neuronal cell populations and are associated with protein aggregates. We reviewed some aspects related to the role of antioxidant properties of Vitamin E in preventing and/or curing neurodegenerative disorders such as the Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, ataxia, tardive dyskinesia and Huntington’s disease.

关键词： Vitamin E neurodegenerative diseases Ataxia with Vitamin E Deficiency

自噬小体绑定化合物(ATTEC)靶向降解线粒体及其潜在治疗效果

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Science Bulletin 2023年第23期68卷 3013-3026,M0006页

作者：谭水霞王达付玉华郑惠文刘妍鲁伯埙 Neurology Department at Huashan Hospital State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceInstitutes of Brain ScienceSchool of Life SciencesFudan UniversityShanghai 200438China Institute for Stem Cell and Neural Regeneration School of PharmacyState Key Laboratory of Reproductive MedicineKey Laboratory of Targeted Intervention of Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjing 211166China

功能异常的线粒体的累积会诱发多种神经退化相关疾病,如帕金森氏病(PD)和唐氏综合征(DS).借助小分子化合物促进线粒体的降解被认为可以缓解这类疾病的进程.然而,目前尚缺乏这样一类高效、安全的靶向降解线粒体的小分子化合物.本研究借... 详细信息

功能异常的线粒体的累积会诱发多种神经退化相关疾病,如帕金森氏病(PD)和唐氏综合征(DS).借助小分子化合物促进线粒体的降解被认为可以缓解这类疾病的进程.然而,目前尚缺乏这样一类高效、安全的靶向降解线粒体的小分子化合物.本研究借助一种名为自噬小体绑定化合物(ATTEC)的新型靶向降解技术,创造性地合成一种能同时结合自噬关键分子LC3B以及线粒体外膜蛋白TSPO的小分子化合物—mT1,并发现该化合物能够有效地降解细胞中的线粒体.借助分子生物学及细胞生物学手段,作者证明mT1能够促进LC3B和TSPO结合,从而将线粒体靶向自噬小体,并进一步与溶酶体融合而降解.此外,在PD的细胞模型和DS的类器官模型中证明mT1能够通过促进线粒体的清除而改善相应的病理学表型.该研究将ATTEC技术的应用范畴拓展到亚细胞器的层面,并为以PD和DS为代表的一类线粒体异常引起的疾病提供了一种潜在的新治疗策略.

关键词： Targeted mitochondrial degradation Autophagy-tethering compounds Chimera compound Lysosome TSPO neurodegenerative diseases

Long non-coding RNAs with essential roles in neurodegenerative disorders

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Neural Regeneration Research 2024年第6期19卷 1212-1220页

作者： Wandi Xiong Lin Lu Jiali Li Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province Kunming Institute of Zoology the Chinese Academy of Sciences Tsinghua-Peking Center for Life Sciences National Institute on Drug Dependence Peking University PKU/McGovern Institute for Brain Research Peking University Institute of Mental Health National Clinical Research Center for Mental Disorders Key Laboratory of Mental Health and Peking University Sixth Hospital Peking University

Recently, with the advent of high-resolution and high-throughput sequencing technologies, an increasing number of long non-coding RNAs(lncRNAs) have been found to be involved in the regulation of neuronal function in the central nervous system with specific spatiotemporal patterns, across different neurodegenerative diseases. However, the underlying mechanisms of lncRNAs during neurodegeneration remain poorly understood. This review provides an overview of the current knowledge of the biology of lncRNAs and focuses on introducing the latest identified roles, regulatory mechanisms, and research status of lncRNAs in Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Finally, this review discusses the potential values of lncRNAs as diagnostic biomarkers and therapeutic targets for neurodegenerative diseases, hoping to provide broader implications for developing effective treatments.

关键词： Alzheimer’s disease amyotrophic lateral sclerosis biomarker Huntington’s disease long non-coding RNAs neurodegenerative diseases Parkinson’s disease therapy transcriptional regulation translational regulation

The Multiple Roles of Autophagy in Neural Function and diseases

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Neuroscience Bulletin 2024年第3期40卷 363-382页

作者： Yan-Yan Li Zheng-Hong Qin Rui Sheng Department of Pharmacology and Laboratory of Aging and Nervous diseases Jiangsu Key laboratory of Neuropsychiatric DiseasesCollege of Pharmaceutical Sciences of Soochow UniversitySuzhou 215123China

Autophagy involves the sequestration and delivery of cytoplasmic materials to lysosomes,where proteins,lipids,and organelles are degraded and recycled.According to the way the cytoplasmic components are engulfed,autophagy can be divided into macroautophagy,microautophagy,and chaperone-mediated autophagy.Recently,many studies have found that autophagy plays an important role in neurological diseases,including Alzheimer's disease,Parkinson's disease,Huntington's disease,neuronal excitotoxicity,and cerebral ischemia.Autophagy maintains cell homeostasis in the nervous system via degradation of misfolded proteins,elimination of damaged organelles,and regulation of apoptosis and inflammation.AMPK-mTOR,Beclin 1,TP53,endoplasmic reticulum stress,and other signal pathways are involved in the regulation of autophagy and can be used as potential therapeutic targets for neurological diseases.Here,we discuss the role,functions,and signal pathways of autophagy in neurological diseases,which will shed light on the pathogenic mechanisms of neurological diseases and suggest novel targets for therapies.

关键词： Autophagy neurodegenerative diseases Cerebral ischemia AMPK mTOR Beclin 1 TP53 Endoplasmic reticulum stress

Effects of bisphenol A and bisphenol analogs on the nervous system

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Chinese Medical Journal 2023年第3期136卷 295-304页

作者： Chunxia Li Chen Sang Shuo Zhang Sai Zhang Hui Gao Department of Obstetrics and Gynecology Beijing Tian Tan HospitalCapital Medical UniversityBeijing 100730China School of Biological Science and Medical Engineering Beihang UniversityBeijing 100191China

Estrogen impacts neural development;meanwhile, it has a protective effect on the brain. Bisphenols, primarily bisphenol A (BPA), can exert estrogen-like or estrogen-interfering effects by binding with estrogen receptors. Extensive studies have suggested that neurobehavioral problems, such as anxiety and depression, can be caused by exposure to BPA during neural development. Increasing attention has been paid to the effects on learning and memory of BPA exposure at different developmental stages and in adulthood. Further research is required to elucidate whether BPA increases the risk of neurodegenerative diseases and the underlying mechanisms, as well as to assess whether BPA analogs, such as bisphenol S and bisphenol F, influence the nervous system.

关键词： Bisphenol A Bisphenol analogs Nervous system Learning/memory disorders neurodegenerative diseases Gender Mechanisms

The regulatory role of Pin1 in neuronal death

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Neural Regeneration Research 2023年第1期18卷 74-80页

作者： Shu-Chao Wang Xi-Min Hu Kun Xiong Center for Medical Research The Second Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina Department of Anatomy and Neurobiology School of Basic Medical SciencesCentral South UniversityChangshaHunan ProvinceChina Hunan Key Laboratory of Ophthalmology ChangshaHunan ProvinceChina

Regulated cell death predominantly involves apoptosis,autophagy,and regulated necrosis.It is vital that we understand how key regulatory signals can control the process of cell death.Pin1 is a cis-trans isomerase that catalyzes the isomerization of phosphorylated serine or threonine-proline motifs of a protein,thereby acting as a crucial molecular switch and regulating the protein functionality and the signaling pathways involved.However,we know very little about how Pin1-associated pathways might play a role in regulated cell death.In this paper,we review the role of Pin1 in regulated cell death and related research progress and summarize Pin1-related pathways in regulated cell death.Aside from the involvement of Pin1 in the apoptosis that accompanies neurodegenerative diseases,accumulating evidence suggests that Pin1 also plays a role in regulated necrosis and autophagy,thereby exhibiting distinct effects,including both neurotoxic and neuroprotective effects.Gaining an enhanced understanding of Pin1 in neuronal death may provide us with new options for the development of therapeutic target for neurodegenerative disorders.

关键词： apoptosis autophagy calpain central nervous system necroptosis necrosis neurodegenerative diseases neuron Pin1 regulated neuronal death

Repurposed anti-cancer epidermal growth factor receptor inhibitors: mechanisms of neuroprotective effects in Alzheimer’s disease

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Neural Regeneration Research 2022年第9期17卷 1913-1918页

作者： Heba M.Mansour Hala M.Fawzy Aiman S.El-Khatib Mahmoud M.Khattab Department of Pharmacology Egyptian Drug AuthorityEDAformerly NODCARGizaEgypt Department of Pharmacology and Toxicology Faculty of PharmacyCairo UniversityCairoEgypt

Numerous molecular mechanisms are being examined in an attempt to discover disease-modifying drugs to slow down the underlying neurodegeneration in Alzheimer’s disease.Recent studies have shown the beneficial effects of epidermal growth factor receptor inhibitors on the enhancement of behavioral and pathological sequelae in Alzheimer’s disease.Despite the promising effects of epidermal growth factor receptor inhibitors in Alzheimer’s disease,there is no irrefutable neuroprotective evidence in well-established animal models using epidermal growth factor receptor inhibitors due to many un-explored downstream signaling pathways.This caused controversy about the potential involvement of epidermal growth factor receptor inhibitors in any prospective clinical trial.In this review,the mystery beyond the under-investigation of epidermal growth factor receptor in Alzheimer’s disease will be discussed.Furthermore,their molecular mechanisms in neurodegeneration will be explained.Also,we will shed light on SARS-COVID-19 induced neurological manifestations mediated by epidermal growth factor modulation.Finally,we will discuss future perspectives and under-examined epidermal growth factor receptor downstream signaling pathways that warrant more exploration.We conclude that epidermal growth factor receptor inhibitors are novel effective therapeutic approaches that require further research in attempts to be repositioned in the delay of Alzheimer’s disease progression.

关键词： Alzheimer’s disease autophagy drug re-positioning epidermal growth factor receptor human epidermal growth factor receptor-2 neurodegenerative diseases neuroinflammation oxidative stress tyrosine kinase inhibitors

Structure,function,and pathology of Neurexin-3

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Genes & diseases 2023年第5期10卷 1908-1919页

作者： Rui Zhang HanXiao Jiang YuanJie Liu GuiQiong He Chongqing Key Laboratory of Neurobiology Chongqing Medical UniversityChongqing 400016China Department of Neurology The Second Affiliated HospitalChongqing Medical UniversityChongqing 400010China Department of Anatomy Chongqing Medical UniversityChongqing 400016China

Neurexin-3 is primarily localized in the presynaptic membrane and forms complexes with various ligands located in the postsynaptic membrane.Neurexin-3 has important roles in synapse development and synapse functions.Neurexin-3 mediates excitatory presynaptic differentiation by interacting with leucine-rich-repeat transmembrane neuronal proteins.Meanwhile,neurexin-3 modulates the expression of presynapticα-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors andγ-aminobutyric acid A receptors by interacting with neuroligins at excitatory and inhibitory synapses.Numerous studies have documented the potential contribution of neurexin-3 to neurodegenerative and neuropsychiatric disorders,such as Alzheimer's disease,addiction behaviors,and other diseases,which raises hopes that understanding the mechanisms of neurexin-3 may hold the key to developing new strategies for related illnesses.This review comprehensively covers the literature to provide current knowledge of the structure,function,and clinical role of neurexin-3.

关键词： Excitatory synapses Inhibitory synapses Neural cell adhesion molecules Neurexin-3 neurodegenerative diseases Neuropsychiatric diseases