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dc.contributor.authorBachor, Tomás P.
dc.contributor.authorKarbanová, Jana.
dc.contributor.authorBüttner, Edgar.
dc.contributor.authorBermúdez, Vicente.
dc.contributor.authorMarquioni-Ramella, Melisa D.
dc.contributor.authorCarmeliet, Peter.
dc.contributor.authorCorbeil, Denis.
dc.contributor.authorSuburo, Angela.
dc.date.accessioned2020-09-22T15:38:40Z
dc.date.available2020-09-22T15:38:40Z
dc.date.issued2017-12-01
dc.identifier.citationNeurobiol Dis 2017 Dec;108:13-28en_US
dc.identifier.issn0969-9961
dc.identifier.urihttps://riu.austral.edu.ar/handle/123456789/947
dc.description.abstractDiabetes mellitus (DM) is reaching epidemic conditions worldwide and increases the risk for cognition impairment and dementia. Here, we postulated that progenitors in adult neurogenic niches might be particularly vulnerable. Therefore, we evaluated the different components of the mouse subventricular zone (SVZ) during the first week after chemical induction of type 1 and type 2 diabetes-like (T1DM and T2DM) conditions. Surprisingly, only T2DM mice showed SVZ damage. The initial lesions were localized to ependymal cilia, which appeared disorientated and clumped together. In addition, they showed delocalization of the ciliary membrane protein prominin-1. Impairment of neuroprogenitor proliferation, neurogenic marker abnormalities and ectopic migration of neuroblasts were found at a later stage. To our knowledge, our data describe for the first time such an early impact of T2DM on the SVZ. This is consistent with clinical data indicating that brain damage in T2DM patients differs from that in T1DM patients.en_US
dc.language.isoenen_US
dc.publisherElsevier Inc. All rights reserved.en_US
dc.subjectCD133en_US
dc.subjectDiabetesen_US
dc.subjectGlucose transporteren_US
dc.subjectNeurogenesisen_US
dc.subjectProminin, Subventricular zoneen_US
dc.subjectNeurodegenerationen_US
dc.titleEarly ciliary and prominin-1 dysfunctions precede neurogenesis impairment in a mouse model of type 2 diabetes.en_US
dc.typeArticleen_US


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