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Nadège Dubourdieu

Researcher at French Institute of Health and Medical Research

Publications -  4
Citations -  134

Nadège Dubourdieu is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Hippocampal formation & Dentate gyrus. The author has an hindex of 3, co-authored 4 publications receiving 72 citations. Previous affiliations of Nadège Dubourdieu include University of Bordeaux.

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Selective dentate gyrus disruption causes memory impairment at the early stage of experimental multiple sclerosis.

TL;DR: It is concluded that early memory impairment in EAE is due to a selective disruption of the dentate gyrus associated with microglia activation, which opens new pathophysiological, imaging, and therapeutic perspectives forMemory impairment in multiple sclerosis.
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Deciphering the microstructure of hippocampal subfields with in vivo DTI and NODDI: Applications to experimental multiple sclerosis.

TL;DR: NODDI maps can help to highlight the internal microanatomy of the hippocampus but NODDI still presents limitations in grey matter as it failed to capture selective dendritic alterations occurring at early stages of a neurodegenerative disease such as multiple sclerosis, whereas DTI maps were significantly altered.
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Aquaporin-4 Surface Trafficking Regulates Astrocytic Process Motility and Synaptic Activity in Health and Autoimmune Disease

TL;DR: It emerges that the membrane dynamics of AQP4 isoform regulate brain cell assemblies in health and autoimmune brain disease targeting AQP3 and human autoantibodies directed against AQp4 from neuromyelitis optica patients impaired AQP 4-M23 dynamic distribution and, consequently, astrocyte process and synaptic activity.
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Complement C3 mediates early hippocampal neurodegeneration and memory impairment in experimental multiple sclerosis.

TL;DR: In early-stage experimental encephalomyelitis (EAE) female mice, the expression level of molecules involved in microglia-neuron interactions within the dentate gyrus and found overexpression of genes of the complement pathway as discussed by the authors.