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dc.contributor.author류훈-
dc.contributor.author손성민-
dc.contributor.author남동우-
dc.contributor.author차문용-
dc.contributor.author김경호-
dc.contributor.author변자영-
dc.contributor.author묵인희-
dc.date.accessioned2021-06-09T03:04:51Z-
dc.date.available2021-06-09T03:04:51Z-
dc.date.issued2015-12-
dc.identifier.citationVOL 36, NO 12-3227-
dc.identifier.issn0197-4580-
dc.identifier.other45920-
dc.identifier.urihttp://pubs.kist.re.kr/handle/123456789/64628-
dc.description.abstractAlzheimer's disease (AD) is characterized by impaired cognitive function and memory loss, which are often the result of synaptic pathology. Thrombospondin (TSP) is an astrocyte-secreted protein, well known for its function as a modulator of synaptogenesis and neurogenesis. Here, we investigated the effects of TSP-1 on AD pathogenesis. We found that the level of TSP-1 expression was decreased in AD brains. When we treated astrocytes with amyloid beta (Aβ), secreted TSP-1 was decreased in autophagy-dependent manner. In addition, treatment with Aβ induced synaptic pathology, such as decreased dendritic spine density and reduced synaptic activity. These effects were prevented by coincubation of TSP-1 with Aβ, which acts through the TSP-1 receptor alpha-2-delta-1 in neurons. Finally, intrasubicular injection with TSP-1 into AD model mouse brains mitigated the Aβ-mediated reduction of synaptic proteins and related signaling pathways. These results indicate that TSP-1 is a potential therapeutic target in AD pathogenesis.-
dc.publisherNeurobiology of aging-
dc.subjectTSP-1-
dc.subjectNeuron-astrocyte crosstalk-
dc.subjectSynaptic dysfunction-
dc.subjectAb-
dc.subjectAlzheimer’s disease (AD)-
dc.titleThrombospondin-1 prevents amyloid beta mediated synaptic pathology in Alzheimer’s disease-
dc.typeArticle-
dc.relation.page32143227-
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