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SUMMARY:BMI SEMINAR // New neurons for old brains : adult neurogenesis in 
 Alzheimer’s disease
DTSTART:20180110T121500
DTEND:20180110T131500
DTSTAMP:20260916T202710Z
UID:19f6d9e7508756f944ea1458fa721da683b24ffd8a03460884f9a481
CATEGORIES:Conferences - Seminars
DESCRIPTION: Claire Rampon\, Revealing Memory Mechanisms of the Brain (RE
 MEMBeR)\, CRCA - UMR 5169 - CNRS\,  Université Paul Sabatier\, Toulouse\
 , France\nAdult hippocampal neurogenesis is strongly impaired in Alzheimer
 ’s disease (AD). In several mouse models of AD\, it was shown that alter
 ed memory performances are associated with hippocampal adult neurogenesis 
 deficits. We have found that adult-born neurons of APPxPS1 mice exhibit re
 duced survival and altered synaptic integration due to a severe lack of de
 ndritic spines. Interestingly\, we revealed that this reduced number of sp
 ines is concomitant of a marked deficit in their neuronal mitochondrial co
 ntent. Remarkably\, by targeting the overexpression of the pro- neural tra
 nscription factor Neurod1 into APPxPS1 adult-born neurons we were able to 
 restores not only their dendritic spine density\, but also their mitochond
 rial content and the proportion of spines associated with mitochondria. Us
 ing primary neurons\, a bona fide model of neuronal maturation\, we identi
 fied that increases of mitochondrial respiration accompany the stimulating
  effect of Neurod1 overexpression on dendritic growth and spine formation.
  Reciprocally\, pharmacologically impairing mitochondria prevented Neurod1
 -dependent trophic effects. Our findings indicate that manipulating mitoch
 ondrial may open new avenues for far-reaching therapeutic implications tow
 ards neurodegenerative diseases associated with cognitive impairment.
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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