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SUMMARY:The Role of the transcriptional regulator PGC-1α in modulating AL
 S
DTSTART:20130903T103000
DTEND:20130903T113000
DTSTAMP:20260916T043945Z
UID:ccbd586f7ee23a32dc5873532cbe31a7903753b403a5759aaccdd0aa
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr. Judith ESCHBACH\nNeurology\, Ulm University (D)\nEschbach 
 J\, Schwalenstöcker B\, Soyal SM\, Bayer H\, Wiesner D\, Akimoto C\, Nils
 son AC\, Birve A\, Meyer T\, Dupuis L\, Danzer KM\, Andersen PM\, Witting 
 A\, Ludolph AC\, Patsch W\, Weydt P.\nAmyotrophic lateral sclerosis (ALS) 
 is a devastating\, adult-onset neurodegenerative disorder of the upper and
  lower motor systems and is associated with muscle wasting and metabolic f
 ailure. The transcriptional co-activator PGC-1α plays an important in the
  regulation of mitochondrial metabolism. Recent evidences from research in
 to Huntington’s disease and Parkinson’s disease suggests that impaired
  function and activity of PGC-1α contributes to the pathogenesis of neuro
 degenerative diseases. In ALS\, PGC-1α overexpression can extend lifespan
  of animal model of ALS\, however\, muscle restricted overexpression of PG
 C-1α has no survival effects. In our study\, we aimed to investigate whet
 her the lack of PGC-1α expression worsens the metabolic and motor phenoty
 pe of ALS transgenic mice\, and whether the loss of PGC-1α has an effect 
 on their survival. Interestingly\, our data show that deletion of PGC-1α 
 leads to an aggravation of the motor phenotype and survival in ALS mice in
  a male specific manner. Such gender differences are also recapitulated in
  ALS patients\, indeed in ALS\, men are affected more often and have an ea
 rlier age of onset than women\, but no underlying mechanisms has been eluc
 idated. Here we report that SNPs in the brain-specific promoter region of 
 the transcriptional co-activator PGC-1α\, modulate age of onset and survi
 val in two large and independent ALS populations in a strictly male-specif
 ic manner.
LOCATION:AI 1142 http://map.epfl.ch/?room=ai1142
STATUS:CONFIRMED
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