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UID:DSC-14402
DTSTART;TZID=Europe/Berlin:20180427T160000
SEQUENCE:1524815947
TRANSP:OPAQUE
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URL:https://www.dresden-science-calendar.de/calendar/de/detail/14402
LOCATION:TUD CRTD\, Fetscherstraße 10501307 Dresden
SUMMARY:Bonifacio: Newborn genetic screening and a primary prevention strat
 egy for Type 1 Diabetes- the Freder1k and POInT study // Cell death in adu
 lt hippocampal neurogenesis is ferroptotic and rescued by selenium
CLASS:PUBLIC
DESCRIPTION:Speaker: Ezio Bonifacio\, Angela Hommel // Gerd Kempermann\, Ta
 ra Walker\nInstitute of Speaker: Postdoc\; Postdoc\nTopics:\nBiologie\, Me
 dizin\n Location:\n  Name: TUD CRTD (CRTD\, auditorium left)\n  Street: Fe
 tscherstraße 105\n  City: 01307 Dresden\n  Phone: +49 (0)351 458 82052\n 
  Fax: +49 (0)351 458 82059 \nDescription: Abstract 1st talk:  The incidenc
 e of childhood type 1 diabetes continues to increase. The vision is to sto
 p this. Therefore\, a Global Platform for the Prevention of Autoimmune Dia
 betes (GPPAD) was initiated. Currently GPPAD runs the Freder1k and the POI
 nT study. Within the Freder1k study\, neonates who are at increased risk t
 o develop type 1 diabetes can now be identified within the newborn screeni
 ng using a type 1 diabetes genetic score. The identified newborns have a g
 reater than 10% risk for pre-symptomatic type 1 diabetes. These families a
 re informed about the meaning of an elevated risk for type 1 diabetes\, ed
 ucated about symptoms of the disease as well as asked to participate in a 
 randomized controlled trial aiming to prevent type 1 diabetes. In this tri
 al called POInT (primary oral Insulin trial)\, children receive a daily do
 se of insulin powder orally to introduce immune tolerance to insulin aimin
 g to prevent type 1 diabetes and create a world without 1 (type 1 diabetes
  that is). The program will screen over 300\,000 newborns to recruit over 
 1000 babies into the trial that lasts for 7.5 years.  Abstract 2nd talk:  
 Apoptotic cell death is a key mechanism controlling the generation of new 
 neurons in the adult hippocampus\, a brain region important for learning a
 nd memory. We show here that ferroptosis\, a recently-discovered form of p
 rogrammed cell death with as yet unknown physiological functions\, explain
 s the first wave of cell death at the precursor cell stage of neurogenesis
 . Reduction of ferroptosis by exogenous selenium increased neurogenesis in
  the hippocampus but not the subventricular zone\, another adult neural st
 em cell niche. This suggests a mechanism whereby external stimuli includin
 g physical activity increase hippocampal but not subventricular zone neuro
 genesis. We propose that ferroptotic elimination maintains an expandable r
 eservoir of neural precursor cells that is sensitive to the environmental 
 regulation of adult hippocampal neurogenesis.
DTSTAMP:20260629T202151Z
CREATED:20180426T080341Z
LAST-MODIFIED:20180427T075907Z
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