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SUMMARY:Improving ER Proteostasis Delays Brain Aging and Age-Related Disea
 ses
DTSTART:20230515T100000
DTEND:20230515T110000
DTSTAMP:20260415T032503Z
UID:78a59f4234f9bcc2b543348d565804cd31d94c0394560d2495bacec6
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Claudio Hetz\, University of Chile and GERO Center for G
 eroscience\, Brain Health and Metabolism\, Santiago (CL) & The Buck Instit
 ute for Research on Aging\, Novato\, CA (USA)\nBIOENGINEERING SEMINAR\n \
 nAbstract:\nAging is the main risk factor to develop neurodegenerative dis
 eases. Alteration in the buffering capacity of the proteostasis network is
  proposed as one of the triggering steps leading to abnormal protein aggre
 gation\, which is also a central hallmark of brain aging.  The endoplasmi
 c reticulum (ER) is a major node of the proteostasis network altered in br
 ain diseases and during aging. ER stress triggers a signaling reaction kno
 wn as the unfolded protein response (UPR)\, which aims at restoring proteo
 stasis through the induction of adaptive programs or the activation of cel
 l death programs when damage is chronic and cannot be repaired. Here I dis
 cuss our efforts to assess the significance of the UPR to brain aging and 
 its contribution to disease\, in addition to develop gene therapy strategi
 es to alleviate ER stress. A new concept is emerging where depending on sp
 ecific UPR component targeted and the disease model tested distinct and ev
 en opposite effects can be observed on the pathology. \n\nThis work was f
 unded by Consolidation Grant – Leading House for the Latin American Regi
 on\, Switzerland\, U.S. Air Force Office of Scientific Research FA9550-21-
 1-0096 (C.H.)\, FONDAP program 15150012\, and Department of Defense grant 
 W81XWH2110960\, FONDEF ID16I10223 and FONDECYT 1220573 (CH)\, ICM-P09-022-
 F (AOA and AGP). FONDEF ID16I10223.\n\n\nBio:\nClaudio Hetz was originally
  trained as Biotechnology Engineer at the University of Chile in Santiago
 \, Chile\, and performed his Ph.D. thesis in Biomedical Sciences at Serono
  Pharmaceutical Research Institute\, Switzerland. This work was performed 
 in the laboratory of Dr. Claudio Soto\, and contributed to defining the ro
 le of ER stress in Prion-related disorders. Hetz then did a postdoctoral t
 raining at Harvard University to study stress responses at the level of pr
 oteostasis control and their relation to disease. This work was supervised
  by Drs Stanley Korsmeyer and Laurie Glimcher\, world leaders in apoptosis
  and ER stress research. He returned to the University of Chile during 200
 7 and is currently Full Professor at the Faculty of Medicine\, in addition
  to holding an adjunct Professor position at the Buck Institute for Resear
 ch in Aging in California and a visiting professor position at Harvard Uni
 versity. He is also currently the Director of the Biomedical Neuroscience 
 Institute (BNI) at the University of Chile\, and associate investigator at
  GERO\, the Center for Geroscience\, Brain health and Metabolism in Santia
 go\, Chile.\n\n\n\nZoom link for attending remotely: https://epfl.zoom.us/
 j/64123266088\n 
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153 https://epfl.zoom.u
 s/j/64123266088
STATUS:CONFIRMED
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