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000138081 1001_ $$0P:(DE-2719)2772760$$aUlusoy, Ayse$$b0$$eFirst author$$udzne
000138081 245__ $$aNeuron-to-neuron α-synuclein propagation in vivo is independent of neuronal injury.
000138081 260__ $$aLondon$$bBiomed Central$$c2015
000138081 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2015-03-24
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000138081 520__ $$aInterneuronal propagation of α-synuclein has been demonstrated in a variety of experimental models and may be involved in disease progression during the course of human synucleinopathies. The aim of this study was to assess the role that neuronal injury or, vice versa, cell integrity could have in facilitating interneuronal α-synuclein transfer and consequent protein spreading in an in vivo animal model.Viral vectors carrying the DNA for human α-synuclein were injected into the rat vagus nerve to trigger protein overexpression in the medulla oblongata and consequent spreading of human α-synuclein toward pons, midbrain and forebrain. Two vector preparations sharing the same viral construct were manufactured using identical procedures with the exception of methods for their purification. They were also injected at concentrations that induced comparable levels of α-synuclein transduction/overexpression in the medulla oblongata. α-Synuclein load was associated with damage (at 6 weeks post injection) and death (at 12 weeks) of medullary neurons after treatment with only one of the two vector preparations. Of note, neuronal injury and degeneration was accompanied by a substantial reduction of caudo-rostral propagation of human α-synuclein.Interneuronal α-synuclein transfer, which underlies protein spreading from the medulla oblongata to more rostral brain regions in this rat model, is not a mere consequence of passive release from damaged or dead neurons. Neuronal injury and degeneration did not exacerbate α-synuclein propagation. In fact, data suggest that cell-to-cell passage of α-synuclein may be particularly efficient between intact, relatively healthy neurons.
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000138081 650_7 $$2NLM Chemicals$$aSNCA protein, human
000138081 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000138081 650_2 $$2MeSH$$aAnimals
000138081 650_2 $$2MeSH$$aBrain: metabolism
000138081 650_2 $$2MeSH$$aDisease Models, Animal
000138081 650_2 $$2MeSH$$aFemale
000138081 650_2 $$2MeSH$$aGene Transfer Techniques
000138081 650_2 $$2MeSH$$aHumans
000138081 650_2 $$2MeSH$$aMedulla Oblongata: metabolism
000138081 650_2 $$2MeSH$$aNerve Degeneration: metabolism
000138081 650_2 $$2MeSH$$aNerve Degeneration: pathology
000138081 650_2 $$2MeSH$$aNeural Pathways: metabolism
000138081 650_2 $$2MeSH$$aNeural Pathways: pathology
000138081 650_2 $$2MeSH$$aNeurons: metabolism
000138081 650_2 $$2MeSH$$aNeurons: pathology
000138081 650_2 $$2MeSH$$aParkinson Disease: metabolism
000138081 650_2 $$2MeSH$$aRats
000138081 650_2 $$2MeSH$$aRats, Sprague-Dawley
000138081 650_2 $$2MeSH$$aalpha-Synuclein: metabolism
000138081 7001_ $$0P:(DE-2719)2810507$$aMusgrove, Ruth E$$b1$$udzne
000138081 7001_ $$0P:(DE-2719)2810495$$aRusconi, Raffaella$$b2$$udzne
000138081 7001_ $$0P:(DE-2719)2810845$$aKlinkenberg, Michael$$b3$$udzne
000138081 7001_ $$0P:(DE-2719)2810665$$aHelwig, Michael$$b4$$udzne
000138081 7001_ $$0P:(DE-2719)2812035$$aSchneider, Anja$$b5$$udzne
000138081 7001_ $$0P:(DE-2719)2481741$$aDi Monte, Donato A$$b6$$eLast author$$udzne
000138081 77318 $$2Crossref$$3journal-article$$a10.1186/s40478-015-0198-y$$b : Springer Science and Business Media LLC, 2015-03-24$$n1$$p13$$tActa Neuropathologica Communications$$v3$$x2051-5960$$y2015
000138081 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-015-0198-y$$gVol. 3, no. 1, p. 13$$n1$$p13$$q3:1<13$$tActa Neuropathologica Communications$$v3$$x2051-5960$$y2015
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