Citations 2
Symposia Report of The Annual Biological Sciences Section Meeting of the Gerontological Society of America 2023, Tampa, Florida
Rogina, Blanka , Anderson, Rozalyn M. , Curan, Sean, Yousefzadeh, Matthew J. , Ghosh, Bhaswati, Duque, Gustavo , Howlett, Susan E. , Austad, Steven N. , Korfhage, Justin , Christensen, Kaare , Carey, James R. , Bell, Justice, Gomes, Ana P. , Dixit, Vishwa Deep , Sen, Payel , Imai, Shin‐ichiro , Valdez, Gregorio , Orr, Miranda E. , Jones, Leanne , Castillo-Azofeida, David, Bonaguidi, Michael A. , Suh, Yousin , Duncan, Francesca E. , C, Weigler G Perry, Burkewitz, Kristopher , Zhou, Kai , Bouhrara, Mustapha , Kolind, Shannon , Dean, Doug, Pálovics, Róbert , Niedernhofer, Laura J. , Fan, Rong , Bueckle, Andreas , Kapahi, Pankaj , Jiang, Nisi , Diaz, Jose , Mishra, Sidharth P. , Ralmundo, Nuno, Banarjee, Reema , Allsopp, Richard , Curran, Sean P. , Anderson, Rozalyn M , Curran, Sean P , Yousefzadeh, Matthew J , Duque, Gustavo , Howlett, Susan , Austad, Steven , Demuth, Ilja , Gerstorf, Denis , Abadir, Peter , Christensen, Kaare , Palmer, Allyson, Basisty, Nathan , de Cabo, Rafael , Sen, Payel , Baur, Joseph A , Duncan, Francesca E , Benjamini, Dan , Walker, Keenan A , Dean, Douglas C , Gladyshev, Vadim N , Fan, Rong , Sato, Shogo , Jiang, Nisi , Ashiqueali, Sarah A., Allsopp, Richard , Niedernhofer, Laura J , Kollind, Shannon H , LeBrasseur, Nathan K. , Lombard, David B. , Alberts, Susan C. , Campos, Fernando A. , Palavicini, Juan Pablo , Palmer, Allyson K. , Basisty, Nathan , Cabo, Rafael de , Baur, Joseph A. , Li, Xiaoling , Pletcher, Scott D. , Andersen, Julie Kay , Jones, Leanne, Suh, Yousin , Murray, Anna , Wang, Meng C., Henne, W. Mike , Walker, Keenan A. , Reiter, David A. , Gorbunova, Vera , Gladyshev, Vadim N. , Hurley, Jennifer , Esser, Karyn A. , Ashiqueali, Sarah , Reynolds, Lindsay M. , Zhang, Bohan , Sebastiani, Paola , Monti, Stefano , Schork, Nicholas J. , Rappaport, Noa
The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences | February 11, 2025 | Volume: 80 | Issue: 5 | Pages: No page available
Abstract The aging process is universal, and it is characterized by a progressive deterioration and decrease in physiological function leading to decline on the organismal level. Nevertheless, a number of genetic and nongenetic interventions have been described, which successfully extend healthspan and lifespan in different species. Furthermore, a number of clinical trials have been evaluating the feasibility of different interventions to promote human health. The goal of the annual Biological Sciences Section of the Gerontological Society of America meeting was to share current knowledge of different topics in aging research and provide a vision of the future of aging research. The meeting gathered international experts in diverse areas of aging research including basic biology, demography, and clinical and translational studies. Specific topics included metabolism, inflammaging, epigenetic clocks, frailty, senescence, neuroscience, stem cells, reproductive aging, inter-organelle crosstalk, comparative transcriptomics of longevity, circadian clock, metabolomics, and biodemography.
Does Declining Mitochondrial NAD+ and Unscheduled Opening of Mitochondrial Transition Pore Promote Mammalian Aging?
Hafner, Angela, Gomes, Ana P. , Liang, Jing , Nair, Sree, Sauve, Anthony A. , Rozenzweig, Anthony, Sinclair, David , Liang, Jing, Cen, Yana , Lanza, Ian R.
Blood | October 12, 2019 | Volume: 116 | Issue: 21 | Pages: SCI-3-SCI-3
10.1182/blood.v116.21.sci-3.sci-3
Abstract Abstract SCI-3 The processes that lead to the susceptibility of post-mitotic tissues to diseases of aging are poorly understood, but mitochondria are considered a key regulator. SIRT3 is mitochondrial sirtuin, a member a family of NAD+-dependent deacetylases. We have previously shown that increased levels of NAD+ in mitochondria promote cell survival in a SIRT3-dependent manner, but how this protection is mediated is unknown. Here we show that mitochondrial NAD+ levels decline dramatically with age and that SIRT3 is a critical component and regulator of the mitochondrial transition pore (MTP). Mice lacking SIRT3 exhibit hyperacetylation of the MTP with age, and as a result, develop multiple defects in post-mitotic tissues as they age, including mitochondrial defects, susceptibility to cardiac failure, and learning and memory deficits. In a mouse model of Alzheimer's disease (AD), SIRT3 knockout mice show striking phenotypes including small size, kyphosis, and a markedly reduced lifespan. Similar to mice, human brain samples show that acetylation of the MTP increases with age and with AD. These findings indicate that declining NAD levels with age lead to memory deficits and accelerate age-related diseases in post-mitotic tissues due to a decline in SIRT3 activity and unscheduled opening of the MTP. Disclosures: Sinclair: GlaxoSmithKline: Consultancy, Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.