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Progress in neurobiology 7건

  1. [해외논문]   Editorial Board   SCI SCIE


    Progress in neurobiology v.165/167 ,pp. ii - ii , 2018 , 0301-0082 ,

    초록

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  2. [해외논문]   Tyrosine hydroxylase as a sentinel for central and peripheral tissue responses in Parkinson's progression: Evidence from clinical studies and neurotoxin models   SCI SCIE

    Johnson, M.E. (School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5000, Australia ) , Salvatore, M.F. (Institute for Healthy Aging and Center for Neuroscience Discovery, University of North Texas Health Science Center, Fort Worth, TX 76107, USA ) , Maiolo, S.A. (School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5000, Australia ) , Bobrovskaya, L. (School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5000, Australia)
    Progress in neurobiology v.165/167 ,pp. 1 - 25 , 2018 , 0301-0082 ,

    초록

    Abstract Parkinson’s disease (PD) is a common neurodegenerative disease worldwide. While the typical motor symptoms of PD are well known, the lesser known non-motor symptoms can also greatly impact the patient’s quality of life. These symptoms often appear before motor impairment, therefore identifying biomarkers that may predict PD risk or pathology has been a major and challenging endeavour. Given that the loss of dopamine, and its rate-limiting enzyme tyrosine hydroxylase (TH) occurs in PD, the expression and accompanying post-translational changes in TH during PD progression could yield insight into the disruption of cellular signalling occurring in the CNS, and also in peripheral tissues wherein catecholamine function plays a role. Furthermore, changes in expression and phosphorylation of TH in the brain and periphery can potentially reveal how TH stability and function are compromised in PD. As such, these changes can reveal how catecholamine synthesis capacity is gradually compromised and how changes in cellular signalling may govern the functional status of remaining catecholaminergic neurons. This review summarises the findings of clinical PD and neurotoxin models of PD that assessed TH expression or phosphorylation in catecholaminergic pathways in the brain and relevant peripheral tissues. We propose that establishing similar changes in TH expression and function in the CNS and periphery of established neurotoxin models can be a potential reference for comparison to changes in TH in human peripheral tissues. These changes in TH expression and phosphorylation may have predictive validity to estimate risk of PD progression before motor impairment is evident. Highlights This review provides a critical analysis of TH regulation in catecholaminergic cells in the brain and periphery in clinical PD and neurotoxin models. We discuss why TH loss is of a different magnitude between the terminal field and somatodendritic compartments of the nigrostriatal pathway in PD. Dynamic changes in TH occur during the loss of catecholaminergic cells in both the brain and relevant peripheral tissues in PD. The possible role of TH phosphorylation in the enzyme’s degradation in PD progression is discussed. Most evidence exists for the 6-OHDA model, as it recapitulates most TH changes in the tissues of interest discussed.

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  3. [해외논문]   Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms   SCI SCIE

    Nokkari, Amaly (Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon ) , Abou-El-Hassan, Hadi (Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon ) , Mechref, Yehia (Department of Chemistry and Biochemistry, Texas Tech University, Lubbock, TX, USA ) , Mondello, Stefania (Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy ) , Kindy, Mark S. (Department of Pharmaceutical Science, College of Pharmacy, University of South Florida, Tampa, FL, USA ) , Jaffa, Ayad A. (Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon ) , Kobeissy, Firas (Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon)
    Progress in neurobiology v.165/167 ,pp. 26 - 50 , 2018 , 0301-0082 ,

    초록

    Abstract Neurological disorders represent major health concerns in terms of comorbidity and mortality worldwide. Despite a tremendous increase in our understanding of the pathophysiological processes involved in disease progression and prevention, the accumulated knowledge so far resulted in relatively moderate translational benefits in terms of therapeutic interventions and enhanced clinical outcomes. Aiming at specific neural molecular pathways, different strategies have been geared to target the development and progression of such disorders. The kallikrein-kinin system (KKS) is among the most delineated candidate systems due to its ubiquitous roles mediating several of the pathophysiological features of these neurological disorders as well as being implicated in regulating various brain functions. Several experimental KKS models revealed that the inhibition or stimulation of the two receptors of the KKS system (B1R and B2R) can exhibit neuroprotective and/or adverse pathological outcomes. This updated review provides background details of the KKS components and their functions in different neurological disorders including temporal lobe epilepsy, traumatic brain injury, stroke, spinal cord injury, Alzheimer’s disease, multiple sclerosis and glioma. Finally, this work will highlight the putative roles of the KKS components as potential neurotherapeutic targets and provide future perspectives on the possibility of translating these findings into potential clinical biomarkers in neurological disease. Highlights The (kallikrein-kinin system) KKS mediates the pathophysiological features of neurological disorders regulating brain functions. The inhibition or stimulation of the KKS receptors (B1R and B2R) can exhibit neuroprotective and/or neuropathological outcomes. The altered KKS dynamics can be utilized as putative biomarkers in different neurological disorders.

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  4. [해외논문]   Uncensored EEG: The role of DC potentials in neurobiology of the brain   SCI SCIE

    Kovac, Stjepana (Department of Neurology and Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Germany ) , Speckmann, Erwin-Josef (Epilepsy Research Center, Westfalische Wilhelms-University Münster, Münster, Germany ) , Gorji, Ali (Department of Neurology and Institute of Translational Neurology, Westfälische Wilhelms-Universität Münster, Germany)
    Progress in neurobiology v.165/167 ,pp. 51 - 65 , 2018 , 0301-0082 ,

    초록

    Abstract Brain direct current (DC) potentials denote sustained shifts and slow deflections of cerebral potentials superimposed with conventional electroencephalography (EEG) waves and reflect alterations in the excitation level of the cerebral cortex and subcortical structures. Using galvanometers, such sustained displacement of the EEG baseline was recorded in the early days of EEG recordings. To stabilize the EEG baseline and eliminate artefacts, EEG was performed later by voltage amplifiers with high-pass filters that dismiss slow DC potentials. This left slow DC potential recordings as a neglected diagnostic source in the routine clinical setting over the last few decades. Brain DC waves may arise from physiological processes or pathological phenomena. Recordings of DC potentials are fundamental electro-clinical signatures of some neurological and psychological disorders and may serve as diagnostic, prognostic, and treatment monitoring tools. We here review the utility of both physiological and pathological brain DC potentials in different aspects of neurological and psychological disorders. This may enhance our understanding of the role of brain DC potentials and improve our fundamental clinical and research strategies for brain disorders. Highlights DC potentials reflect changes in the level of excitation of the Brain. DC potentials induce by physiological or pathological brain activities. Several brain disorders produce abnormalities in physiological DC brain activity. Pathological DC brain waves have been observed in several neurological disorders. Monitoring of DC potentials may serve as diagnostic, prognostic, and treatment monitoring tools.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  5. [해외논문]   Cell adhesion and matricellular support by astrocytes of the tripartite synapse   SCI SCIE

    Hillen, Anne E.J. (Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands ) , Burbach, J. Peter H. (Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands ) , Hol, Elly M. (Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands)
    Progress in neurobiology v.165/167 ,pp. 66 - 86 , 2018 , 0301-0082 ,

    초록

    Abstract Astrocytes contribute to the formation, function, and plasticity of synapses. Their processes enwrap the neuronal components of the tripartite synapse, and due to this close interaction they are perfectly positioned to modulate neuronal communication. The interaction between astrocytes and synapses is facilitated by cell adhesion molecules and matricellular proteins, which have been implicated in the formation and functioning of tripartite synapses. The importance of such neuron-astrocyte integration at the synapse is underscored by the emerging role of astrocyte dysfunction in synaptic pathologies such as autism and schizophrenia. Here we review astrocyte-expressed cell adhesion molecules and matricellular molecules that play a role in integration of neurons and astrocytes within the tripartite synapse. Highlights Astrocytes are regulators of synapse formation and function. Cell adhesion and matricellular molecules expressed by astrocytes promote synaptogenesis. Cell adhesion and matricellular molecules expressed by astrocytes contribute to the tripartite function.

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  6. [해외논문]   Role of cellular prion protein in interneuronal amyloid transmission   SCI SCIE

    del Rí (Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of Science and Technology, Barcelona, Spain ) , o, José (Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Barcelona, Spain ) , A. (Molecular and Cellular Neurobiotechnology, Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of Science and Technology, Barcelona, Spain) , Ferrer, Isidre , Gaví , n, Rosalina
    Progress in neurobiology v.165/167 ,pp. 87 - 102 , 2018 , 0301-0082 ,

    초록

    Abstract Several studies have indicated that certain misfolded amyloids composed of tau, β-amyloid or α-synuclein can be transferred from cell to cell, suggesting the contribution of mechanisms reminiscent of those by which infective prions spread through the brain. This process of a ‘prion-like’ spreading between cells is also relevant as a novel putative therapeutic target that could block the spreading of proteinaceous aggregates throughout the brain which may underlie the progressive nature of neurodegenerative diseases. The relevance of β-amyloid oligomers and cellular prion protein (PrP C ) binding has been a focus of interest in Alzheimer’s disease (AD). At the molecular level, β-amyloid/PrP C interaction takes place in two differently charged clusters of PrP C . In addition to β-amyloid, participation of PrP C in α-synuclein binding and brain spreading also appears to be relevant in α-synucleopathies. This review summarizes current knowledge about PrP C as a putative receptor for amyloid proteins and the physiological consequences of these interactions. Highlights PrP C can bind to different amyloid (β-sheet-rich) proteins. Amyloid-interacting PrP C domains comprise two charged cluster domains (CC1 and 2). PrP C participates in the expansion of amyloid (at least α-synuclein) deposits in wild-type mice.

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  7. [해외논문]   Notch signaling and neuronal death in stroke   SCI SCIE

    Arumugam, Thiruma V. (Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore ) , Baik, Sang-Ha (Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore ) , Balaganapathy, Priyanka (Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore ) , Sobey, Christopher G. (Department of Physiology, Anatomy & Microbiology, School of Life Sciences, La Trobe University, Melbourne, Victoria, Australia ) , Mattson, Mark P. (Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA ) , Jo, Dong-Gyu (School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea)
    Progress in neurobiology v.165/167 ,pp. 103 - 116 , 2018 , 0301-0082 ,

    초록

    Abstract Ischemic stroke is a leading cause of morbidity and death, with the outcome largely determined by the amount of hypoxia-related neuronal death in the affected brain regions. Cerebral ischemia and hypoxia activate the Notch1 signaling pathway and four prominent interacting pathways (NF-κB, p53, HIF-1α and Pin1) that converge on a conserved DNA-associated nuclear multi-protein complex, which controls the expression of genes that can determine the fate of neurons. When neurons experience a moderate level of ischemic insult, the nuclear multi-protein complex up-regulates adaptive stress response genes encoding proteins that promote neuronal survival, but when ischemia is more severe the nuclear multi-protein complex induces genes encoding proteins that trigger and execute a neuronal death program. We propose that the nuclear multi-protein transcriptional complex is a molecular mediator of neuronal hormesis and a target for therapeutic intervention in stroke. Highlights We review the roles of Notch in the neuropathology of ischemic stroke. We discuss the mechanisms for how Notch interacts with other gene transcription regulators such as HIF-1α, NF-κB, p53 and Pin1 following a stroke. We introduce a novel concept of a multi-protein complex which controls the expression of genes that determine the fate of neurons in stroke. We discuss if and how the multi-protein complex may regulate neuronal plasticity and resilience during the remodeling phase following stroke. We conclude with a perspective on how this research may lead to novel approaches for clinical intervention in ischemic stroke.

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