Bonn Lab Study Shows Blood Cells From Older Donors Lose Epigenetic Age in a Dish

THE ARISING · LONGEVITY & HEALTHSPAN SUNDAY, OCTOBER 18, 2026 IN THIS EDITION · LONGEVITY & HEALTHSPAN 1 ACOG Now Recommends Hormone Therapy for Many Women With Hot Flashes 2 Cardiologists Urge Doctors to Prescribe Exercise as Routine Heart Care 3 Fasting and Autophagy in Humans: Summary Calls Link Unproven 4 Gut Supplements May Modestly Improve Cognition in Adults Over 60, Review Finds 5 Higher Ultra-Processed Food Intake Linked to Silent Brain Damage on MRI 6 Higher VO2 Max Linked to Lower Depression and Anxiety Risk in UK Biobank 7 Bonn Lab Study Shows Blood Cells From Older Donors Lose Epigenetic Age in a Dish 8 Longer Sleep Linked to Kidney Disease Risk in Type 2 Diabetes LONGEVITY & HEALTHSPAN · WEEKLY READ · 3 MIN AGING CELL · 2 SOURCES Bonn Lab Study Shows Blood Cells From Older Donors Lose Epigenetic Age in a Dish Blood cells from very old donors can be converted in a dish into neural stem cells whose DNA-based age reads far younger, but nothing in this work turns back the age of a person. The widely quoted figure that cells from an 80-year-old reached a molecular age under 20 comes from press coverage, not from the study text we have. he study, published in Aging Cell in 2026 by Berg and colleagues at the University of Bonn and partner institutions, is laboratory research on humanT cells. It did not involve animals or patients. The text available to us does not state how many donors were used. It says only that donors ranged from newborns to people aged 101. The team took red blood cell precursors from donor blood. They added two genes, SOX2 and cMYC, using a virus. This pushed the cells to become induced neural stem cells, which can go on to form brain cells. Unlike the more common route, the cells did not first pass through a pluripotent stage, in which a cell can become almost any tissue. THE ARISING · OCTOBER 18, 2026 PAGE 19 To estimate age, the researchers used an epigenetic clock. This is a computer method that reads chemical tags on DNA, called methylation, which change with age. The tags do not alter the genetic code. They affect how often genes are read. According to the study, neural stem cells made from older donors kept only about 13% of the donor's original age at low passages, meaning early rounds of cell growth. At high passages, meaning many rounds of growth, they kept about 5%. By our arithmetic, 13% of 80 years is roughly 10 years. The new finding is about timing. The age reset was not instant. It continued for several weeks, and it continued even when conditions were set to block cell division. Differences in gene activity between young and old donors' cells also faded with more time in conversion. The authors say the established cell lines lacked age- associated cellular hallmarks, much like cells made through the pluripotent route. The cells also took a long time to settle into a true neural stem cell identity. According to the paper, that process went on well after the first cells with a neural stem cell marker, PAX6, appeared. The press release, as carried by AZO Life Sciences, reports that cells from an 80-year- old came out with a molecular age below 20. It quotes Prof. Oliver Brüstle of the University Hospital of Bonn saying the slow pace makes it possible to "investigate which factors and active substances accelerate or slow down the rejuvenation process." The coverage's headline mentions 50 days, while its text says the change could be tracked for over 100 days. The study's abstract says only "several weeks," so the exact timeline is unclear from what we have. FOR YOU What does this mean for readers? Not much yet, and the limits matter. The study's own introduction notes that methylation age is a proxy for biological age. It is not a direct measure of how well cells work. The coverage says the rejuvenation makes cells "actually behave like young cells," but the abstract supports a narrower claim: the cell lines lack age-associated hallmarks. The cells were also not the same cells that were taken from the donors. They were changed into a different cell type, grown in dishes, and treated with viral vectors. Nothing here shows that an aging body, or even an aging organ, can be reset. The study tested no treatment, drug or supplement. THE ARISING · OCTOBER 18, 2026 PAGE 20 The practical value is in research. A slow reset is easier to watch step by step than a fast one. It may help scientists find what drives epigenetic aging and whether it can be sped up or slowed down. Age is the main risk factor for diseases such as Alzheimer's, which is why Brüstle says the model matters for neuroscience. The work was funded by the EU's Horizon 2020 programme, the German Research Foundation and Germany's federal research ministry, according to the coverage. Next, watch for follow-up work that identifies which molecules speed up or slow the reset, and whether any of those findings hold up in living tissue. Sources: Aging cell (2026), AZO Life Sciences (reporting University of Bonn study in Aging Cell) THE ARISING · OCTOBER 18, 2026 PAGE 21