Investigating the impact of Dasatinib, Quercetin, and Fisetin on DNA aging markers in a study on anti-aging interventions.
In a groundbreaking study published in Aging (Albany NY), researchers delved into the effects of Dasatinib, Quercetin, and Fisetin on DNA methylation clocks as part of a longitudinal investigation into senolytic interventions. Senolytics, compounds targeting cellular senescence, have shown promise in enhancing health span, yet their impact on epigenetic age has remained largely unexplored. The team, comprised of scientists from the Institute For Hormonal Balance, TruDiagnostic, Buck Institute for Research on Aging, and Cornell University, aimed to unravel the intricate relationship between senolytic treatments and DNA methylation, epigenetic age, and immune cell subsets.
The study was structured into two phases to comprehensively assess the effects of senolytic drugs on epigenetic aging. The first phase involved a pilot study where 19 participants underwent a 6-month treatment regimen of Dasatinib and Quercetin (DQ), with DNA methylation measurements taken at baseline, 3 months, and 6 months. Intriguingly, the results revealed significant increases in epigenetic age acceleration in first-generation epigenetic clocks and mitotic clocks at the 3-month and 6-month marks, accompanied by a noticeable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks, indicating a nuanced impact of the treatment on different facets of epigenetic aging.
Building upon these initial findings, the subsequent phase of the study introduced Fisetin into the treatment regimen, combining it with DQ to form DQF. Over the course of a year, 19 participants - including 10 from the initial study - received the DQF treatment for 6 months, with DNA methylation assessments conducted at baseline and 6 months. Surprisingly, the addition of Fisetin to the regimen resulted in non-significant increases in epigenetic age acceleration, hinting at a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging. This observation underscores the complex interplay between different senolytic compounds and their influence on the aging process at the molecular level.
One of the key insights derived from the study was the notable differences in immune cell proportions between the DQ and DQF treatment groups. This divergence in immune cell subsets provides a biological basis for the distinct patterns observed in the evolution of epigenetic clocks under the two treatment conditions. These findings not only shed light on the intricate mechanisms underlying senolytic interventions but also highlight the need for further research to validate and fully grasp the implications of combining these interventions for promoting healthy aging and longevity.
In conclusion, this longitudinal study represents a significant step forward in understanding the effects of senolytic treatments on DNA methylation clocks and epigenetic age. By unraveling the complex interactions between Dasatinib, Quercetin, Fisetin, and their impact on cellular aging processes, the researchers have laid the groundwork for future investigations aimed at harnessing the potential of senolytics for enhancing overall health and well-being in aging populations.
Source: https://www.eurekalert.org/news-releases/1036819
The study was structured into two phases to comprehensively assess the effects of senolytic drugs on epigenetic aging. The first phase involved a pilot study where 19 participants underwent a 6-month treatment regimen of Dasatinib and Quercetin (DQ), with DNA methylation measurements taken at baseline, 3 months, and 6 months. Intriguingly, the results revealed significant increases in epigenetic age acceleration in first-generation epigenetic clocks and mitotic clocks at the 3-month and 6-month marks, accompanied by a noticeable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks, indicating a nuanced impact of the treatment on different facets of epigenetic aging.
Building upon these initial findings, the subsequent phase of the study introduced Fisetin into the treatment regimen, combining it with DQ to form DQF. Over the course of a year, 19 participants - including 10 from the initial study - received the DQF treatment for 6 months, with DNA methylation assessments conducted at baseline and 6 months. Surprisingly, the addition of Fisetin to the regimen resulted in non-significant increases in epigenetic age acceleration, hinting at a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging. This observation underscores the complex interplay between different senolytic compounds and their influence on the aging process at the molecular level.
One of the key insights derived from the study was the notable differences in immune cell proportions between the DQ and DQF treatment groups. This divergence in immune cell subsets provides a biological basis for the distinct patterns observed in the evolution of epigenetic clocks under the two treatment conditions. These findings not only shed light on the intricate mechanisms underlying senolytic interventions but also highlight the need for further research to validate and fully grasp the implications of combining these interventions for promoting healthy aging and longevity.
In conclusion, this longitudinal study represents a significant step forward in understanding the effects of senolytic treatments on DNA methylation clocks and epigenetic age. By unraveling the complex interactions between Dasatinib, Quercetin, Fisetin, and their impact on cellular aging processes, the researchers have laid the groundwork for future investigations aimed at harnessing the potential of senolytics for enhancing overall health and well-being in aging populations.
Source: https://www.eurekalert.org/news-releases/1036819
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