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Does abnormal brain development contribute to late onset neurological conditions?| old_uid | 15692 |
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| title | Does abnormal brain development contribute to late onset neurological conditions? |
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| start_date | 2018/04/13 |
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| schedule | 12h-12h30 |
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| online | no |
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| details | Un temps d'échanges entre Carmen Sandi et les doctorants et post-doctorants récemment recrutés par NeuroCog, sera organisé de 13h à 14h. |
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| summary | The bulk of interest in the HTT (HTT) protein has centered on the fact that, when mutated, HTT causes Huntington’s disease (HD), a devastating neurological disorder. The mutation causing HD is an abnormal polyglutamine stretch in HTT. Given the adult onset and dysfunction and death of adult neurons characterizing HD, most studies have focused on the toxic effects elicited by mutant HTT in post-mitotic neurons. However, the protein is ubiquitous and expressed in the developing embryo where it plays an essential role as revealed by the early embryonic lethality at day 7.5 of the complete knockout of the HTT gene in mouse. Anyway, the roles of the wild-type protein during development have been overlooked. I will discuss how HTT regulates several steps of mouse embryonic corticogenesis. HTT is important to maintain the pool of cycling progenitors and also regulates the polarization of newly generated neurons. I will describe the underlying molecular mechanisms by which HTT mediates its effects. Finally, I will also show the consequences of the presence of an abnormal polyglutamine expansion in HTT during cortical neurogenesis and consider the viewing of HD as a developmental disorder. |
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| responsibles | Sadoul |
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