A triple drug combination has been used to extend the lifespan of fruit flies by 48% in a new study led by UCL and the Max Planck Institute for Biology of Ageing.

The three drugs are all already in use as medical treatments: lithium as a mood stabiliser, trametinib as a cancer treatment and rapamycin as an immune system regulator.

The findings, published in Proceedings of the National Academy of Sciences (PNAS), suggest that a combination drug treatment may one day be helpful at preventing age-related diseases in people.

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A follow on study from their previous human trial targeting IPF. This time the researchers ran a study to see how senolytics influenced diabetic kidney disease and if it actually removes senescent cells in humans.

Senescent cells, which can release factors that cause inflammation and dysfunction, the senescence-associated secretory phenotype (SASP), accumulate with ageing and at etiological sites in multiple chronic diseases. Senolytics, including the combination of Dasatinib and Quercetin (D + Q), selectively eliminate senescent cells by transiently disabling pro-survival networks that defend them against their own apoptotic environment. In the first clinical trial of senolytics, D + Q improved physical function in patients with idiopathic pulmonary fibrosis (IPF), a fatal senescence-associated disease, but to date, no peer-reviewed study has directly demonstrated that senolytics decrease senescent cells in humans.

Reference

Hickson, L. J., Prata, L. G. L., Bobart, S. A., Evans, T. K., Giorgadze, N., Hashmi, S. K., … & Kellogg, T. A. (2019). Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease. EBioMedicine.

At our 2019 Ending Age-related Diseases conference in New York City, we had the pleasure of speaking with Dr. Michael West, the CEO of AgeX Therapeutics.

Dr. West can rightfully be called a pioneer in his field with a substantial background in biomedical and biotechnology corporations. After completing his PhD at Baylor College of Medicine, he founded Geron Corporation in 1990, where he launched and directed programs in telomere biology as it relates to cancer, aging, and human embryonic stem cell technology. He subsequently established the research group that went on to isolate human embryonic stem cells for the first time.

After his time at Geron, Dr. West was chairman and CEO of Advanced Cell Technology, which was acquired by the Japanese company Astellas Pharma in 2016 for $379 Million. Following his success with Advanced Cell Technology and Geron, Dr. West served as the CEO/co-CEO of BioTime Inc. for ten years.

Aging is the biggest risk factor for cancer, but the mechanisms linking these two processes remain unclear. Using GTEx and TCGA data, we compared genes differentially expressed with age and genes differentially expressed in cancer among nine human tissues. In most tissues, aging and cancer gene expression pattern changed in the opposite direction. The exception was thyroid and uterus, where we found transcriptomic changes in the same direction in aging and in their corresponding cancers. The overlapping sets between genes differentially expressed with age and genes differentially expressed in cancer across tissues were enriched for several processes, mainly cell cycle and the immune system. Moreover, cellular senescence signatures, derived from a meta‐analysis, changed in the same direction as aging in human tissues and in the opposite direction of cancer signatures. Therefore, transcriptomic changes in aging and in cellular senescence might relate to a decrease in cell proliferation, while cancer transcriptomic changes shift toward enhanced cell division. Our results highlight the complex relationship between aging and cancer and suggest that, while in general aging processes might be opposite to cancer, the transcriptomic links between human aging and cancer are tissue‐specific.

Researchers at the Buck Institute, including Dr. Judy Campisi, have published a new study that shows, for the first time, that senescent cells are associated with age-related blood clots [1].

As we get older, increasing numbers of our cells enter into a state known as cellular senescence. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals known as the senescence-associated secretory phenotype (SASP), which encourages nearby healthy cells to enter the same senescent state.

The presence of high levels of SASP reduces tissue repair, increases chronic inflammation, and can even raise the risk of cancer and other age-related diseases.