Matthew O'Connor

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College for T Cells
In a new study, late-life treatment with a three-element senolytic vaccine led to lower senescence markers and a 12% increase in median lifespan in female B6 mice. However, short-lived controls complicate the picture [1]. Helping the immune system kill “zombie cells” Cellular SenescenceAs your body ages, more of your cells become senescent. Senescent cells do...
Astrocytes
In Aging Cell, researchers have described how increasing fibroblast growth factor 13 (FGF13) in astrocytes reduces aging throughout the bodies of mice. A factor from a well-known family FGFs are signaling molecules that share structural and functional commonalities and play crucial roles in biology, including neural function [1]. Some of these molecules are secreted, and...
RNA DNA Interaction
A recent study identified SRSF1, an RNA-processing and splicing factor, as a molecule with geroprotective potential. Inducing SRSF1 expression rejuvenated human cells in vitro, extended lifespan, and significantly reduced frailty in mice [1]. Alternative approaches Differentiated cells have the capacity to rejuvenate if an appropriate molecular environment is provided. The best-known factors that enable cellular...
One of the oldest and biggest longevity conferences moved this year across the Atlantic, from Copenhagen to Boston. The new location brought ARDD close to several important longevity hubs and might have contributed to this edition’s practical, entrepreneurial, and forward-oriented spirit. We have already reported on the unprecedented panel where FDA named longevity a priority....
Life Biosciences
Life Biosciences (“Life Bio”), a biotechnology company pioneering cellular rejuvenation medicines to reverse diseases of aging, announced interim data from its Phase 1 clinical trial of ER-100 in three participants with open angle glaucoma (OAG). The data demonstrated that a single intravitreal administration along with daily oral doxycycline was well-tolerated through Day 56 in all...
Regulatory Bottleneck 1
Researchers are developing biomedical repair therapies to address multiple age-related diseases at once, yet they are forced to put them through regulatory pathways built for single-disease drugs. The result is delay, duplication, and unnecessary cost precisely when speed matters the most. The single-disease-indication trap Current regulation still treats age-related diseases as if they were a...