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Food Science and Human Wellness 2024年第2期13卷 1093-1107页

作者： Yu Xi Wenhui Li Junru Wang Meihong Yu Xiangquan Zeng He Li Jian Li Key Laboratory of Green and Low-Carbon Processing Technology for Plant-Based Food of China National Light Industry Council Beijing Advanced Innovation Center for Food Nutrition and Human HealthBeijing Technology and Business UniversityBeijing 100048China

Trimethyltin chloride(TMT)is a potent neurotoxin to cause neurodegeneration,especially in *** study aimed to identify dietary components that can effectively attenuate TMT-induced neurodegeneration in *** predominant anthocyanin in human diets,cyanidin-3-O-glucoside(C3G,5 or 50 mg/kg),was given to mice for 16 days,and TMT(2.7 mg/kg)was injected intraperitoneally once on the eighth day.C3G(50 mg/kg)significantly alleviated TMT-induced seizures and subsequent cognitive impairment by ameliorating hippocampal neurodegeneration and synaptic ***,C3G treatment restored glutamate homeostasis in brain and reversed glutamine synthetase(GS)inhibition in reactive astrogliosis and neuroinflammation,which are critical for C3G's neuroprotective ***,C3G decreased the lipopolysaccharide,tumor necrosis factor-α,interleukin-6,and interleukin-1βlevels in the mice,which potentially by modulating the relative abundance of Atopobiaceae and Lachnospiraceae in the gut.C3G may be a promising and practical dietary component for reducing TMT-induced neurodegeneration.

关键词： Cyanidin-3-O-glucoside Trimethyltin neurodegeneration Glutamatergic pathway Gut microbiota

Role of neuroinflammation in neurodegeneration development

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Signal Transduction and Targeted Therapy 2023年第8期8卷 3649-3680页

作者： Weifeng Zhang Dan Xiao Qinwen Mao Haibin Xia Laboratory of Gene Therapy Department of BiochemistryCollege of Life SciencesShaanxi Normal University199 South Chang’an RoadXi’an 710062P.R.China The State Laboratory of Cancer Biology Department of Biochemistry and Molecular BiologyAir Force Medical UniversityNo.169 Changle West RoadXi’an 710032P.R.China Department of Burns and Cutaneous Surgery Xijing HospitalAir Force Medical UniversityNo.169 Changle West RoadXi’an 710032China Department of Pathology University of UtahHuntsman Cancer Institute2000 Circle of Hope DriveSalt Lake CityUT 84112USA

Studies in neurodegenerative diseases,including Alzheimer’s disease,Parkinson’s disease and Amyotrophic lateral sclerosis,Huntington’s disease,and so on,have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this *** aggregates which are very common pathological phenomenon in neurodegeneration can induce neuroinflammation which further aggravates protein aggregation and ***,inflammation even happens earlier than protein *** induced by genetic variations in CNS cells or by peripheral immune cells may induce protein deposition in some susceptible *** signaling pathways and a range of CNS cells have been suggested to be involved in the pathogenesis of neurodegeneration,although they are still far from being completely *** to the limited success of traditional treatment methods,blocking or enhancing inflammatory signaling pathways involved in neurodegeneration are considered to be promising strategies for the therapy of neurodegenerative diseases,and many of them have got exciting results in animal models or clinical *** of them,although very few,have been approved by FDA for clinical *** we comprehensively review the factors affecting neuroinflammation and the major inflammatory signaling pathways involved in the pathogenicity of neurodegenerative diseases,including Alzheimer’s disease,Parkinson’s disease,and Amyotrophic lateral *** also summarize the current strategies,both in animal models and in the clinic,for the treatment of neurodegenerative diseases.

关键词： inflammation neurodegeneration Huntington

Novel therapeutic strategies targeting mitochondria as a gateway in neurodegeneration

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Neural Regeneration Research 2023年第5期18卷 991-995页

作者： Diogo Trigo Jose Joao Vitoria Odete A.B.da Cruz e Silva Neuroscience and Signalling Laboratory Institute of Biomedicine(iBiMED)Department of Medical SciencesUniversity of AveiroAveiroPortugal

In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that have a variety of functions in ensuring cellular health and homeostasis. The plethora of mitochondrial functionalities confers them an intrinsic susceptibility to internal and external stressors(such as mutation accumulation or environmental toxins), particularly so in long-lived postmitotic cells such as neurons. Thus, it is reasonable to postulate an involvement of mitochondria in aging-associated neurological disorders, notably neurodegenerative pathologies including Alzheimer’s disease and Parkinson’s disease. On the other hand, biological effects resulting from neurodegeneration can in turn affect mitochondrial health and function, promoting a feedback loop further contributing to the progression of neuronal dysfunction and cellular death. This review examines state-of-the-art knowledge, focus on current research exploring mitochondrial health as a contributing factor to neuroregeneration, and the development of therapeutic approaches aimed at restoring mitochondrial homeostasis in a pathological setting.

关键词： Alzheimer’s disease axon energy homeostasis glymphatic system mitochondria mitostasis neurodegeneration neuroregeneration Parkinson’s disease therapeutical strategies

Neurodevelopmental defects as a primer of neurodegeneration:lessons from spinal muscular atrophy and Huntington's disease

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Neural Regeneration Research 2023年第9期18卷 1952-1953页

作者： Stuart J.Grice Ji-Long Liu Medical Research Council Functional Genomics Unit Department of PhysiologyAnatomy and GeneticsUniversity of OxfordOxfordUK School of Life Science and Technology ShanghaiTech UniversityShanghaiChina

Developmental motifs in neurodegeneration:neurodegeneration,the prominent feature of neurodegenerative disease,is characterized by the progressive and selective loss of neuronal *** some of the pathologies caused by neurodegeneration may be irreversible,early intervention will be required for the treatments that aim to slow or halt the manifestation of these ***,neurodegeneration evokes the idea of a progressive decline of brain function.

关键词： neurodegeneration Huntington function

Elevated phosphorylated ubiquitin level elicits neurodegeneration by aggregating the decline of ubiquitindependent proteasomal degradation

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中国药理学与毒理学杂志 2023年第7期37卷 516-517页

作者： CHEN Cong GAO Tongyao WANG Tong LU Yunbi ZHANG Weiping Department of Pharmacology School of Medicine Zhejiang University

OBJECTIVE To determine the roles of phosphorylated ubiquitin(pUb) on ubiquitin-dependent proteasomal(UPS) degradation activity, and the roles of pUb on neurodegeneration. METHODS We use PTEN induced kinase 1(PINK1) to phosphorylate ubiquitin. The Ub/S65A cannot be phosphorylated by PINK1, and was used to antagonize the roles of pUb. The Ub/S65E was used to mimic the roles of pUb. The roles of pUb on UPS degradation activity were determined by immunofluorescence, Western blot and TIRF microscope at cellular and protein level. The roles of pUb on neurodegeneration were determined by behavior tests, immunofluorescence,Golgi staining, TEM, Western blot and proteomics sacle in mouse. RESULTS The level of soluble PINK1(sPINK1)and pUb increased in the neurons of aged mouse brain,and in the cells upon the administration of MG132, a proteasome inhibitor. The elevation of sPINK1 and pUb was accompanied by protein aggregation upon aging or the proteasomal inhibition. The pink1 knockout alleviated proteasomal inhibition induced protein aggregation and association of ubiquitinated proteins with *** over-expression of sPINK1 increased pUb level in hippocampal neuron, which chronically induced protein aggregation, mitochondrial damage and damage the structure of neuronal spines. Such neuronal injury lead to cognitive impairment of mice. The roles of sPINK1 was reversed by co-expression with Ub/S65A, and was mimic by over-expression with Ub/S65E. CONCLUSION The phosphorylation of ubiquitin aggravates UPS degradation, and accelerates neuronal degeneration upon the decline of proteasomal degradation in aging and agerelated neuronal diseases.

关键词： aging neurodegeneration phosphorylated ubiquitin proteasome protein aggregation PTEN induced kinase 1

neurodegeneration in Diabetic Retinopathy： Current Concepts and Therapeutic Implications

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Chinese Medical Journal 2016年第24期129卷 3001-3003页

作者： Ning-Li Wang Beijing Institute of Ophthalmology Beijing Tongren Eye Center Beijing Tongren Hospital Capital Medical University Beijing Key Laboratory of Ophthalmology and Visual Sciences Beijing 100005 China

The prevalence of diabetes mellitus （DM） has increased significantly in recent decades in China. Recently, it has been reported that the estimated prevalence of DM among a representative sample of Chinese adults was 11.6% and the prevalence of prediabetes was 50.1%. Furthermore, the awareness, treatment, and control rates of DM in the general Chinese population are disproportionately low, raising concerns for future high rates of diabetes-related morbidity and mortality.

关键词： Diabetic Retinopathy neurodegeneration Neuroprotection

Dexmedetomidine mitigates isoflurane-induced neurodegeneration in fetal rats during the second trimester of pregnancy

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Neural Regeneration Research 2017年第8期12卷 1329-1337页

作者： Zhi-yuan Su Qing Ye Xian-bao Liu Yu-zhong Chen Hong Zhan Shi-yuan Xu Department of Anesthesia The Third Affiliated Hospital of Guangzhou Medical University Department of Anesthesia Zhujiang Hospital of Southern Medical University

Dexmedetomidine has significant neuroprotective effects. However, whether its protective effects can reduce neurotoxicity caused by isoflurane in fetal brain during the second trimester of pregnancy remains unclear. In this study, timed-pregnancy rats at gestational day 14 spontaneously inhaled 1.5% isoflurane for 4 hours, and were intraperitoneally injected with dexmedetomidine at dosages of 5, 10, 20, and 20 μg/kg 15 minutes before inhalation and after inhalation for 2 hours. Our results demonstrate that 4 hours after inhaling isoflurane, 20 μg/kg dexmedetomidine visibly mitigated isoflurane-induced neuronal apoptosis, reversed downregulation of brain-derived neurotrophic factor expression, and lessened decreased spatial learning and memory ability in adulthood in the fetal rats. Altogether, these findings indicate that dexmedetomidine can reduce neurodegeneration induced by isoflurane in fetal rats during the second trimester of pregnancy. Further, brain-derived neurotrophic factor participates in this process.

关键词： nerve regeneration dexmedetornidine isoflurane fetal rat apoptosis brain-derived neurotrophic factor behavior neuroprotection neurodegeneration neural regeneration

Sarm1-mediated neurodegeneration within the enteric nervous system protects against local inflammation of the colon

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Protein & Cell 2021年第8期12卷 621-638页

作者： Yue Sun Qi Wang Yi Wang Wenran Ren Ying Cao Jiali Li Xin Zhou Wei Fu Jing Yang State Key Laboratory of Membrane Biology School of Life SciencesCenter for Life SciencesPeking UniversityBeijing 100871China IDG/McGovem Institute for Brain Research Peking UniversityBeijing 100871China Chinese Institute for Brain Research Beijing 102206China Shenzhen Bay Laboratory Institute of Molecular PhysiologyShenzhen 518055China Department of General Surgery Peking University Third HospitalBeijing 100191China School of Medicine Tsinghua UniversityBeijing 100084China Kunming Institute of Zoology Chinese Academy of SciencesKunming 650223China

Axonal degeneration is one of the key features of neu-rodegenerative *** the canonical view,axonal degeneration destructs neural connections and promotes detrimental disease ***,we assessed the enteric nervous system(ENS)of the mouse,nonhuman primate,and human by advanced 3D *** observed the profound neurodegeneration of catecholaminergic axons in human colons with ulcerative colitis,and similarly,in mouse colons during acute dextran sulfate sodium-induced ***,we unexpectedly revealed that blockage of such axonal degeneration by the Sarml deletion in mice exacerbated the colitis *** contrast,pharmacologic ablation or chemogenetic inhibition of catecholaminergic axons suppressed the colon *** further showed that the catecholaminergic neurotransmitter norepinephrine exerted a pro-inflammatory function by enhancing the expression of IL-17 ***,this study demonstrated that Sarm1-mediated neurodegeneration within the ENS mitigated local inflammation of the colon,uncovering a previously-unrecognized beneficial role of axonal degeneration in this disease context.

关键词： 3D imaging enteric nervous system axonal degeneration neurodegeneration catecholaminergic axons Sarm1 colitis

Tau hyperphosphorylation induces apoptotic escape and triggers neurodegeneration in Alzheimer's disease

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Neuroscience Bulletin 2014年第2期30卷 359-366页

作者： Jian-Zhi Wang Zhi-Hao Wang Qing Tian Department of Pathology and Pathophysiology Key Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical College Huazhong University of Science and Technology

Since abnormal post-translational modifications or gene mutations of tau have been detected in over twenty neurodegenerative disorders, tau has attracted widespread interest as a target protein. Among its various post-translational modifications, phosphorylation is the most extensively studied. It is recognized that tau hyperphosphorylation is the root cause of neurodegeneration in Alzheimer＇s disease （AD）; however, it is not clear how it causes neurodegeneration. Based on the findings that tau hyperphosphorylation leads to the escape of neurons from acute apoptosis and simultaneously impairs the function of neurons, we have proposed that the nature of AD neurodegeneration is the consequence of aborted apoptosis induced by tau phosphorylation. Therefore, proper manipulation of tau hyperphosphorylation could be promising for arresting AD neurodegeneration. In this review, the neuroprotective and neurodegenerative effects of tau hyperphosphorylation and our thoughts regarding their relationship are presented.

关键词： Alzheimer's disease microtubule-associated protein tau hyperphosphorylaUon apoptosis neurodegeneration

Tau-induced neurodegeneration: mechanisms and targets

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Neuroscience Bulletin 2014年第2期30卷 346-358页

作者： Cindy Beharry Leah S. Cohen Jing Di Kawsar Ibrahim Susan Briffa-Mirabella Alejandra del C. Alonso Department of Biology and Center for Developmental Neuroscience College of Staten Island Graduate Center The City University of New York

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau＇s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications： hyperphosphorylation, ubiquitination, glycation, glycosytation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau＇s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.

关键词： tau phosphorylation neurodegeneration tauopathies mitochondria microtubules tubulinkinases phosphatases Alzheimer's disease