يعرض 1 - 10 نتائج من 53 نتيجة بحث عن '"GAP-43"', وقت الاستعلام: 1.55s تنقيح النتائج
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    المؤلفون: Seehusen, Frauke Antje

    مصطلحات موضوعية: Abschlussarbeit, Habilitation, ddc:630, Verzeichnis wissenschaftlicher Veröffentlichungen, Hochschulbibliographie allgemein, Demyelinating diseases of the central nervous system are an etiologically heterogeneous group, in which a primary loss of myelin is accompanied by preservation of the axonal integrity. In the last years, there was a paradigm shift in multiple sclerosis in humans as well as in its animal models like canine distemper virus (CDV) infection. Nevertheless, the pathogenesis of axonopathies and the influence of several cellular and acellular factors on axonal growth promoting or inhibitory properties were not investigated so far. Additionally, in diseases with neurological deficits and a suspected genetic mutation as a possible cause a detailed characterization on a molecular and morphological level is often missing. New therapeutical strategies in demyelinating diseases include potentially remyelinating aldynoglial cells, also known as central Schwann cells. In the introduction, an overview concerning the structure of axons, axonal transport, relevance of axonopathies in inflammatory and degenerative diseases of the central nervous system (CNS) is given followed by a description of the neurotrophin receptor p75NTR and its expression in several differentiation stages in Schwann cells. The influence of remyelinating Schwann cells as a regenerative process on neurodegenerative processes is briefly described. In addition, the canine and murine diseases (canine distemper virus infection, granulomatous meningoencephalitis [GME], neuroaxonal dystrophy [NAD], Theiler`s murine encephalomyelitis [TME] and dystonia musculorum) investigated in this habilitation were delineated. The aim was the comparative contemplation of different naturally occurring and experimentally induced CNS diseases using several in situ and in vitro methods. The ten publications summarized in this thesis can be allocated to six aims: 1. Characterization of the pathogenesis of axonal damage in CDV-induced demyelinating leukoencephalitis 2. Characterization of changes in the quality and quantity of extracellular matrix in CDV-induced demyelinating leukoencephalitis 3. Description and characterization of p75NTR-positive Schwann cells in the brain of dogs with CDV-induced demyelinating leukoencephalitis and GME 4. Characterization of neurodegenerative changes in a new variant of NAD based on a mutation in the canine tectonin beta-propeller repeat-containing protein 2 (TECPR2) gene 5. Characterization of the pathogenesis of axonopathies in TME 6. Characterization of neurodegenerative changes in a new variant of murine dystonia musculorum In canine distemper demyelinating leukoencephalitis, an increased immunoreactivity of non-phosphorylated neurofilament, a marker for damaged axons, was accompanied by loss of cytoskeletal and motor proteins. In contrast to the results on the protein level, transcriptional upregulation of genes, which code for neurofilament subunits and motor proteins, was detected in chronic lesions compared to subacute lesions. Immunohistochemically, hints for regeneration were obvious, consisting of axonal immunoreactivity for HIF1α. Nevertheless, GAP-43, erythropoietin and its receptor showed no regulation or were downregulated. The extracellular matrix (ECM) is regarded as a mainly axonal growth inhibitory factor. In CDV-infected dogs, changes in the quality and quantity of the ECM were detected compared to controls. Aggrecan expression was upregulated in early and late lesions, whereas the expression of collagen type I and IV as well as fibronectin was upregulated mainly in late lesions. In contrast

    وصف الملف: 1 Online-Ressource (XI, 199 Seiten)

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    مرشدي الرسالة: Silva, Kátia Karina do Monte, Costa, Belmira Lara da Silveira Andrade da

    المصدر: Repositório Institucional da UFPEUniversidade Federal de PernambucoUFPE.

    مصطلحات موضوعية: ETCC anódica, Córtex cerebral, Microglia, GAP-43, Astrócitos

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