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  1. Book ; Online ; Thesis: Development of viral tools for CNS gene transfer: Adeno-Associated Viral Vectors in gene therapy of Parkinson's disease

    Shevtsova, Zinayida

    2006  

    Abstract: Gene transfer to the brain is a promising therapeutic strategy for a variety of neurodegenerative disorders including Parkinson’s disease (PD). PD is characterized by a progressive degeneration of the nigrostriatal dopaminergic system. By using adeno- ... ...

    Author's details vorgelegt von Zinayida Shevtsova
    Abstract Gene transfer to the brain is a promising therapeutic strategy for a variety of neurodegenerative disorders including Parkinson’s disease (PD). PD is characterized by a progressive degeneration of the nigrostriatal dopaminergic system. By using adeno-associated viral (AAV) vector that allows for long-term and stable transgene expression, a single intervention rather than continuous pharmacological treatment may provide a therapeutic effect. In this study, BclXL and GDNF have been evaluated separately and in combination as prospective neuroprotective molecules for gene therapy in the complete 6-hydroxydopamine lesion model of PD. Efficiency of gene therapy is dependent on the effective transduction of the selected regions in the brain. AAV-2 serotype is known to preferentially transduce dopaminergic neurons in substantia nigra (SN) and therefore was chosen for BclXL and/or GDNF gene transfer into this region ...
    Language English
    Size Online-Ressource, Ill., graph. Darst
    Publisher Niedersächsische Staats- und Universitätsbibliothek
    Publishing place Göttingen
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Univ., Diss.--Göttingen, 2002
    Database Former special subject collection: coastal and deep sea fishing

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  2. Book ; Online ; Thesis: Development of viral tools for CNS gene transfer

    Shevtsova, Zinayida [Verfasser]

    adeno-associated viral vectors in gene therapy of Parkinson's disease

    2006  

    Author's details submitted by Zinayida Shevtsova
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Evaluation of long-term upregulation of Calbindin D28K as a preventive approach for ischaemic stroke.

    Freimann, Florian B / Crome, Olaf / Shevtsova, Zinayida / Bähr, Mathias / Kügler, Sebastian

    International journal of stroke : official journal of the International Stroke Society

    2010  Volume 5, Issue 4, Page(s) 319–320

    Abstract: Buffering of intracellular calcium peaks following an acute ischaemic stroke protects neurons from necrotic and apoptotic cell death. However, the need for on-demand delivery of protective agents due to the short therapeutic window in stroke therapy ... ...

    Abstract Buffering of intracellular calcium peaks following an acute ischaemic stroke protects neurons from necrotic and apoptotic cell death. However, the need for on-demand delivery of protective agents due to the short therapeutic window in stroke therapy makes it difficult to apply a calcium-buffering strategy in patients. We investigated the effects of a preventive upregulation of the calcium-binding protein Calbindin D28K as a potential approach for patients at a high risk of ischaemic stroke. We overexpressed Calbindin D28K in the striatal and cortical region in mice using an adeno-associated viral vector (AAV) for 12 weeks, and then assessed neuroprotective effects after MCAO. In contrast to studies showing a neuroprotective effect of shortly induced Calbindin D28K overexpression, we found no increased survival of neurons overexpressing Calbindin D28K for 12 weeks.We suggest that neuronal calcium metabolism adapts to higher Calbindin D28K levels after long-term overexpression. This potentially preventive approach to protect from ischaemic stroke does not have clinical applicability.
    MeSH term(s) Animals ; Brain/pathology ; Brain Ischemia/complications ; Brain Ischemia/pathology ; Brain Ischemia/prevention & control ; Calbindin 1 ; Calbindins ; Calcium/metabolism ; Cerebral Cortex/metabolism ; Dependovirus ; Fluorescent Dyes ; Genetic Therapy ; Green Fluorescent Proteins/biosynthesis ; Green Fluorescent Proteins/genetics ; Infarction, Middle Cerebral Artery/pathology ; Infarction, Middle Cerebral Artery/prevention & control ; Mice ; Necrosis ; Neostriatum/metabolism ; Risk ; S100 Calcium Binding Protein G/biosynthesis ; Stroke/etiology ; Stroke/pathology ; Stroke/prevention & control ; Up-Regulation
    Chemical Substances Calb1 protein, mouse ; Calbindin 1 ; Calbindins ; Fluorescent Dyes ; S100 Calcium Binding Protein G ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2010-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2303728-3
    ISSN 1747-4949 ; 1747-4930
    ISSN (online) 1747-4949
    ISSN 1747-4930
    DOI 10.1111/j.1747-4949.2010.00446.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CNS-expressed cathepsin D prevents lymphopenia in a murine model of congenital neuronal ceroid lipofuscinosis.

    Shevtsova, Zinayida / Garrido, Manuel / Weishaupt, Jochen / Saftig, Paul / Bähr, Mathias / Lühder, Fred / Kügler, Sebastian

    The American journal of pathology

    2010  Volume 177, Issue 1, Page(s) 271–279

    Abstract: Deficiency in Cathepsin D (CtsD), the major cellular lysosomal aspartic proteinase, causes the congenital form of neuronal ceroid lipofuscinoses (NCLs). CtsD-deficient mice show severe visceral lesions like lymphopenia in addition to their central ... ...

    Abstract Deficiency in Cathepsin D (CtsD), the major cellular lysosomal aspartic proteinase, causes the congenital form of neuronal ceroid lipofuscinoses (NCLs). CtsD-deficient mice show severe visceral lesions like lymphopenia in addition to their central nervous system (CNS) phenotype of ceroid accumulation, microglia activation, and seizures. Here we demonstrate that re-expression of CtsD within the CNS but not re-expression of CtsD in visceral organs prevented both central and visceral pathologies of CtsD(-/-) mice. Our results suggest that CtsD was substantially secreted from CNS neurons and drained from CNS to periphery via lymphatic routes. Through this drainage, CNS-expressed CtsD acts as an important modulator of immune system maintenance and peripheral tissue homeostasis. These effects depended on enzymatic activity and not on proposed functions of CtsD as an extracellular ligand. Our results furthermore demonstrate that the prominent accumulation of ceroid/lipofuscin and activation of microglia in brains of CtsD(-/-) are not lethal factors but can be tolerated by the rodent CNS.
    MeSH term(s) Animals ; Cathepsin D/genetics ; Cathepsin D/metabolism ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Ceroid/metabolism ; Dependovirus/genetics ; Dependovirus/metabolism ; Disease Models, Animal ; Genetic Vectors ; Humans ; Lymphopenia/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/metabolism ; Neuronal Ceroid-Lipofuscinoses/metabolism ; Neuronal Ceroid-Lipofuscinoses/pathology ; Neurons/metabolism ; Survival Rate ; Thymus Gland/cytology ; Tissue Distribution ; Viscera/metabolism ; Viscera/pathology
    Chemical Substances Ceroid ; Cathepsin D (EC 3.4.23.5)
    Language English
    Publishing date 2010-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.2353/ajpath.2010.091267
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.76: Show issues Location:
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