Improving ER Proteostasis Delays Brain Aging and Age-Related Diseases
Event details
| Date | 15.05.2023 |
| Hour | 10:00 › 11:00 |
| Speaker | Prof. Claudio Hetz, University of Chile and GERO Center for Geroscience, Brain Health and Metabolism, Santiago (CL) & The Buck Institute for Research on Aging, Novato, CA (USA) |
| Location | Online |
| Category | Conferences - Seminars |
| Event Language | English |
BIOENGINEERING SEMINAR
Abstract:
Aging is the main risk factor to develop neurodegenerative diseases. Alteration in the buffering capacity of the proteostasis network is proposed as one of the triggering steps leading to abnormal protein aggregation, which is also a central hallmark of brain aging. The endoplasmic reticulum (ER) is a major node of the proteostasis network altered in brain diseases and during aging. ER stress triggers a signaling reaction known as the unfolded protein response (UPR), which aims at restoring proteostasis through the induction of adaptive programs or the activation of cell death programs when damage is chronic and cannot be repaired. Here I discuss our efforts to assess the significance of the UPR to brain aging and its contribution to disease, in addition to develop gene therapy strategies to alleviate ER stress. A new concept is emerging where depending on specific UPR component targeted and the disease model tested distinct and even opposite effects can be observed on the pathology.
This work was funded by Consolidation Grant – Leading House for the Latin American Region, 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.
Bio:
Claudio 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 role of ER stress in Prion-related disorders. Hetz then did a postdoctoral training at Harvard University to study stress responses at the level of proteostasis 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 2007 and is currently Full Professor at the Faculty of Medicine, in addition to holding an adjunct Professor position at the Buck Institute for Research in Aging in California and a visiting professor position at Harvard University. 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 Santiago, Chile.
Zoom link for attending remotely: https://epfl.zoom.us/j/64123266088
Abstract:
Aging is the main risk factor to develop neurodegenerative diseases. Alteration in the buffering capacity of the proteostasis network is proposed as one of the triggering steps leading to abnormal protein aggregation, which is also a central hallmark of brain aging. The endoplasmic reticulum (ER) is a major node of the proteostasis network altered in brain diseases and during aging. ER stress triggers a signaling reaction known as the unfolded protein response (UPR), which aims at restoring proteostasis through the induction of adaptive programs or the activation of cell death programs when damage is chronic and cannot be repaired. Here I discuss our efforts to assess the significance of the UPR to brain aging and its contribution to disease, in addition to develop gene therapy strategies to alleviate ER stress. A new concept is emerging where depending on specific UPR component targeted and the disease model tested distinct and even opposite effects can be observed on the pathology.
This work was funded by Consolidation Grant – Leading House for the Latin American Region, 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.
Bio:
Claudio 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 role of ER stress in Prion-related disorders. Hetz then did a postdoctoral training at Harvard University to study stress responses at the level of proteostasis 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 2007 and is currently Full Professor at the Faculty of Medicine, in addition to holding an adjunct Professor position at the Buck Institute for Research in Aging in California and a visiting professor position at Harvard University. 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 Santiago, Chile.
Zoom link for attending remotely: https://epfl.zoom.us/j/64123266088
Practical information
- Informed public
- Free
Organizer
Contact
- Marie Rodriguez