TimePie (focus on anti-aging science)

We’re seeing China’s booming longevity industry & its rapid evolution. Day 2|#7thTimePieLongevityForum Beyond understanding why we age, the focus is shifting toward how longevity clinics work, how to integrate with healthcare system, how longevity tech can be part of daily life.

A study evaluated the 5-year effect of #aspirin on a modified Intrinsic Capacity (IC) index in older males and females. Low-dose aspirin did not prevent functional decline and was linked to a small additional decline in IC in older females. By Joanne Ryan, @prof_horvath et al.

@prof_horvath paper:

A new way to boost protein degradation could widen the reach of targeted therapies for complex neurodegenerative diseases. @RapeLab team identified the reductive stress-response E3 ligase CUL2FEM1B; its activation restores mitochondrial function and neuronal survival.

A bi-adjuvant #senolytic nanovaccine targeting dendritic cell senescence improves aging-related metabolic dysfunction. In multiple aged mouse models, CK5-GC-NV cleared Gpnmb+ senescent adipocytes, improved metabolism, and extended lifespan. Paper:

In conversation with @xprize Healthspan Finalist @ut_godalab's clinical partner, Tokyo ReLife Clinic — on their “#SuperExosome” tech that aims to reverse 10+ years of age-related decline. From 600+ teams, what got them into the Top 10? Full interview:

Why does #proteostasis fail in the aging brain? @AOri_lab et al. suggest reversible oxidation of catalytic cysteines in deubiquitylases may be partly to blame. Age-related redox imbalance can impair these enzymes, disrupt ubiquitin homeostasis, and drive proteostasis decline.

@AOri_lab The paper highlighted the oxidation sensitivity of deubiquitylases as amplifiers of brain aging, and discussed whether restoring thiol homeostasis could help maintain ubiquitin-dependent protein quality control in the aging brain.

The cardiovascular resilience of #centenarians does not come from an absence of aging or disease, but from a delayed onset of cardiovascular pathology and the preservation of the body’s adaptive compensatory capacity. A new review led by @pmcbastos:

Shandong Quanxi Biotech, a biotechnology company from China, finds evidence that muscle stem cell treatment mitigates stress-associated multiorgan dysfunction in accelerated aging mice and improves behavior in naturally aged mice. #MuSCs #aging

A senescence-modulating therapeutic strategy for #uterine #aging: Ginsenoside Rb1 Rather than selectively eliminating senescent cells, Rb1 primarily targets senescence-associated dysfunction and restores endometrial homeostasis. Paper:

Richard Miller: 7 ways not to think carefully about aging 1.there is a cause 2.each person has a biological age and can be measured 3.cells have an age 4.old cells can rejuvenate 5.biomarkers of age measure aging rate 6.lifespan vs healthspan 7.hallmarks of aging collection

Blood proteins linked to mortality also track with biological ageing across organ systems Study of 2,100+ participants identifies 17 mortality-associated plasma proteins and independently replicates key findings in an #aging cohort. By Nicholas Garvey, @NirBarzilaiMD, et al.

@NirBarzilaiMD paper:

What happens inside endothelial cells as we age, why does their function decline? @rooij_laura is investigating this by studying tissues classified as healthy or non-diseased, focusing on molecular changes driven by aging itself, rather than those linked to diagnosed disease.

@rooij_laura paper:

South Korean scientists identified a novel age-associated antimicrobial peptide (AMP), #Pileup, in aging Drosophila. Beyond its classic role in microbial defense, Pileup may also help clear #senescent host cells, preserving #gut #homeostasis.

Long-lived species don’t just burn energy more slowly — they have better-tuned metabolisms that protect mitochondria and boost stress resistance, helping cells stay healthy for centuries. Shown in a study of bivalves living 30 to 500+ years.

Human T-cell receptor (#TCR) diversity doesn’t decline at a steady rate — it drops more sharply after age 50, and men generally have lower diversity than women. Chronic CMV infection further reduces TCR diversity, roughly equivalent to an extra 20 years of #immune #aging.

Nonlinear Aging of the Human TCR Repertoire Is Influenced by Sex, CMV, and Cancer By @nbirkbak team