BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Memento EPFL//
BEGIN:VEVENT
SUMMARY:BMI Seminar // Huntington’s disease: from gene identification to
  gene therapy
DTSTART:20130515T121500
DTEND:20130515T131500
DTSTAMP:20260921T021040Z
UID:9b1dc9c427323181efea9f6e455253590ce15f92ca545f74d95b2490
CATEGORIES:Conferences - Seminars
DESCRIPTION:Nicole Déglon\nLaboratory of Cellular and Molecular Neurother
 apies\nNeuoligie\, Faculté de biologie et médecine\, Lausanne\, Switzerl
 and\nAbstract\nHuntington’s disease (HD) is an autosomal dominant neurod
 egenerative disorder disease that affects 1 in 10\,000 adults. The symptom
 s\, which include progressive motor\, psychiatric and cognitive dysfunctio
 ns\, are associated with the degeneration of the major population of stria
 tal neurons\, the GABAergic spiny projection neurons. In 1983\, the huntin
 gtin (HTT) gene was the first disease gene mapped to a specific chromosome
 . Ten years later the precise nature of the HD-associated mutation was ide
 ntified as an expansion of CAG repeats in the HTT gene. Despite intensive 
 efforts devoted to investigating the mechanisms of its pathogenesis\, effe
 ctive treatments for this devastating disease remain unavailable. Disease-
 modifying treatments are being investigated that may lead to disease-alter
 ing therapies. However\, the most attractive strategy for the treatment of
  HD is certainly RNAi. Gene-silencing techniques that target polyglutamine
 -encoding mRNA and block or reduce the production of mutant Htt protein\, 
 have the potential to halt or\, at least\, delay neuronal death and theref
 ore constitute a promising strategy for HD. Recent data providing evidence
  of the therapeutic potential\, as well as advantages and limitations of n
 on allele- or allele-specific RNAi for HD will be presented.
LOCATION:SV1717A
STATUS:CONFIRMED
END:VEVENT
END:VCALENDAR