Happening today at 1 PM, NRB 350. Please join us! https://t.co/lwspYfMq2J

🌟 Congratulations to @LudgerGoeminne and the @gladyshev_lab team on their recent publication in @Cell_Metabolism! The study reveals insights into organ-specific aging clocks and their links to disease risk and lifestyle. #Aging #Proteomics Read here:

Your biological age should NOT be ONE number. Introducing Ageome: our new framework that measures aging across thousands of molecular pathways simultaneously 🧬. Ageome challenges the single-number paradigm of biological age, offering a high-dimensional view of aging across

🧵5/5: 🙏 Big thanks to all involoved @JPCastro_Aging, @AnastasiaShind, @KejunYing, @MarcoOnATree, @dobry_gremlin, @CsabaKerepesi, Aleksandr Tyshkovskii and all our fantastic collaborators! #ACBCs #BcellLymphoma #Aging #CancerResearch

🧵4/5: 🌍 While mouse and human B cell lymphomas differ, the epigenetic changes we observed in mice align with those in humans, suggesting potential intervention strategies.

🧵3/5: 🔬 ACBCs thrive independently, support malignancy in young recipients, and shorten lifespan. Excitingly, longevity interventions in old mice reduced these pre-malignant changes!

🧵2/5: 🧬 We uncovered how aging drives mouse B cell lymphoma development via c-Myc activation, promoter hypermethylation, and somatic mutations. These changes lead to the expansion of age-associated clonal B cells (ACBCs) and increased biological age.

🧵1/5: Thrilled to share our latest paper in @NatureAging ! https://t.co/SwLSfVAGDd

10/10: We greatly acknowledge the hard work of our team, our excellent collaborators, and the studies of other labs in the aging field.

9/10: Together, our analyses increase our understanding of the basis of epigenetic clocks and highlight potential opportunities for targeting aging and evaluating longevity interventions.

8/10: We noted that aging clocks may favor select stochastic changes as major predictive features due to the properties of penalized regressions typically used for building such clocks.

7/10: Moreover, we found a co-regulated component likely linked with programmatic aging changes across at least two levels of regulation — DNA methylation and gene expression.

6/10: We found a notable contribution of stochastic accumulation of aging changes in both DNA methylation and gene expression aging signals.

5/10: In our study, we sought to delineate stochastic and co-regulated components of aging changes by analyzing single-cell DNA methylation and gene expression. To do so, we analyzed aging dynamics of these signals in single cells during aging and development in mice.

4/10:In the same Nature Aging issue, two other groups published studies confirming our results ("Aging clocks based on accumulation of stochastic variation" by @Meyer_DH @schumacherbj, and "Quantifying the stochastic component of epigenetic aging" by H. Tong and A. Teschendorff)

3/10: Over 10 years ago, precise epigenetic clocks predicting human age were developed, however, the mechanistic explanation for their work was not fully clear.

2/10: Herein, we evaluate the contributions of stochastic and co-regulated components to single-cell epigenetic and transcriptomic aging in mice.

1/10: We are pleased to announce that our manuscript on the nature of epigenetic aging from a single-cell perspective is now published in Nature Aging:

When does a human organismal life begin? Aging may provide a clue! https://t.co/TSWs3TiOBP

🧵9/9: We greatly acknowledge the hard work of our team, our excellent collaborators, and the works of other labs in the partial reprogramming field.