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CHOROID PLEXUS DYSFUNCTION AND ITS IMPACT ON CORTICAL PLASTICITY TIMING IN HUNTINGTON DISEASE
Fanny Namysland 4 co-authors
Institut du Cerveau - Paris Brain Institute, Sorbonne Université, INSERM, CNRS, APHP - Hôpital de la Pitié Salpêtrière
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-289
Presentation
Date TBA
Board: PS05-09AM-289
Event Information
Poster Board
PS05-09AM-289
Poster
View posterAbstract
During early post-natal development of Huntington Disease (HD) animal models, cortical networks are transiently altered but normalize within a few weeks yet leading to symptoms in adulthood. This transient window of defective circuitry resembles a critical period of plasticity, when neuronal networks strengthen after maturation of parvalbumin-expressing interneurons. Maturation is triggered when parvalbumin-expressing interneurons internalize the OTX2 transcription factor, which is secreted by the choroid plexus into the cerebrospinal fluid and delivered to the cortex.
As mislocalisation or disruption of tight junction proteins has been observed in different epithelia in HD, I hypothesized that the integrity of the choroid plexus may be compromised in HD, affecting cortical development and maintenance. Using a knock-in HD mouse model, I found decreased expression levels of junctional proteins at juvenile and adult stages, and alterations in the morphology and structure of epithelial cells from the choroid plexus. I also studied maturation hallmarks in the cortex, which appears to be accelerated in HD compared to the control group. Future studies will assess whether this arises from an altered distribution of OTX2 from the dysfunctional plexus choroid to the cortex.
As mislocalisation or disruption of tight junction proteins has been observed in different epithelia in HD, I hypothesized that the integrity of the choroid plexus may be compromised in HD, affecting cortical development and maintenance. Using a knock-in HD mouse model, I found decreased expression levels of junctional proteins at juvenile and adult stages, and alterations in the morphology and structure of epithelial cells from the choroid plexus. I also studied maturation hallmarks in the cortex, which appears to be accelerated in HD compared to the control group. Future studies will assess whether this arises from an altered distribution of OTX2 from the dysfunctional plexus choroid to the cortex.
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