info:eu-repo/semantics/article
Early ciliary and prominin-1 dysfunctions precede neurogenesis impairment in a mouse model of type 2 diabetes
Fecha
2017-12Registro en:
Bachor, Tomás Pedro; Karbanová, Jana; Büttner, Edgar; Bermúdez, Vicente; Marquioni Ramella, Melisa Daniela; et al.; Early ciliary and prominin-1 dysfunctions precede neurogenesis impairment in a mouse model of type 2 diabetes; Academic Press Inc Elsevier Science; Neurobiology of Disease; 108; 12-2017; 13-28
0969-9961
CONICET Digital
CONICET
Autor
Bachor, Tomás Pedro
Karbanová, Jana
Büttner, Edgar
Bermúdez, Vicente
Marquioni Ramella, Melisa Daniela
Carmeliet, Peter
Corbeil, Denis
Suburo, Angela Maria
Resumen
Diabetes 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.