Citations 2
The Fourth Annual Symposium of the Midwest Aging Consortium
Kim, Jinoh , Buffenstein, Rochelle , Vanegas, Natalia-Del Pilar , Agudelo-Garcia, Paula A., Rojas, Mauricio , Englund, Davis A. , Nunes, Allancer , Kohut, Marian L. , Kothadiya, Siddhant , Bardhan, Rizia , Camell, Christina D. , Sturmlechner, Ines , Lamming, Dudley W. , Leiser, Scott F. , Escorcia, Wilber , Gill, Matthew S. , Helfand, Stephen L., Korm, Sovannarith , Pehar, Mariana , Blaszkiewicz, Magdalena , McGregor, Eric R. , Stilgenbauer, Lukas , Taylor, Alicia , McNeill, Elizabeth M. , Sturmlechner, Ines , Lamming, Dudley W , Anderson, Rozalyn M , Bai, Hua , Englund, Davis A. , Bronikowski, Anne M. , Rosas, Lorena , Mora, Ana Lucia , LeBrasseur, Nathan K. , Robbins, Paul D. , Goronzy, Jörg J. , Yeh, Chung‐Yang , Huang, Shijiao , Taylor, Jackson R. , Gribble, Kristin E. , Townsend, Kristy L. , Anderson, Rozalyn M. , Sadagurski, Marianna , Stoeger, Thomas
The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences | November 5, 2024 | Volume: 79 | Issue: 11 | Pages: No page available
Abstract The Midwest Aging Consortium (MAC) has emerged as a critical collaborative initiative aimed at advancing our understanding of aging and developing strategies to combat the rising prevalence of age-related diseases. Founded in 2019, MAC brings together researchers from various disciplines and institutions across the Midwestern United States to foster interdisciplinary geroscience research. This report summarizes the highlights of the Fourth Annual Symposium of MAC, which was held at Iowa State University in May 2023. The symposium featured presentations on a wide array of topics, including studies on slow-aging animals, cellular senescence and senotherapeutics, the role of the immune system in aging, metabolic changes in aging, neuronal health in aging, and biomarkers for measuring the aging process. Speakers shared findings from studies involving a variety of animals, ranging from commonly used species such as mice, rats, worms, yeast, and fruit flies, to less-common ones like naked mole-rats, painted turtles, and rotifers. MAC continues to emphasize the importance of supporting emerging researchers and fostering a collaborative environment, positioning itself as a leader in aging research. This symposium not only showcased the current state of aging biology research but also highlighted the consortium’s role in training the next generation of scientists dedicated to improving the healthspan and well-being of the aging population.
P44, the ‘longevity‐assurance’ isoform of P53, regulates tau phosphorylation and is activated in an age‐dependent fashion
Pehar, Mariana , Ko, Mi Hee, Scrable, Heidi, Puglielli, Luigi , Li, Mi
Aging Cell | December 17, 2013 | Volume: 13 | Issue: 3 | Pages: 449-456
Summaryp44 is a short isoform of p53 with ‘longevity‐assurance’ activity. Overexpression of p44 in the mouse (p44+/+ transgenic mice) causes a progeroid phenotype that mimics an accelerated form of aging. The phenotype includes abnormal phosphorylation of the microtubule‐binding protein tau, synaptic deficits, and cognitive decline. Genetic engineering demonstrated that the phosphorylation status of tau acts upstream of the synaptic deficits. Here, we provide evidence that p44 promotes the phosphorylation of tau in the mouse. Specifically, we show that p44 binds to the promoter of tau kinases Dyrk1A, GSK3β, Cdk5, p35, and p39 and activates their transcription. The upregulation of the above kinases is followed by increased phosphorylation of tau. Finally, we show that p44 is preferentially found in the nucleus and that its levels increase with age in the mouse brain. Taken together, these results suggest that an imbalance in the p53:p44 ratio might be involved with the altered tau metabolism that characterizes aging.