Max Planck Retractions Expose Algorithmic Risks in Publishing: A strange Retraction Watch listing led historians Yves Gingras and Mahdi Khelfaoui to discover that Springer Nature had quietly retracted two Max Planck papers from the 1940s for alleged copyright violations. The researchers argue the decision applies modern publishing norms anachronistically to an era when scholars commonly reused essays across journals to reach different audiences. One retracted piece had appeared elsewhere, but the other seems to have been flagged because it shared a title with a critical essay by philosopher Aloys Müller, even though the contents differed. The journal’s editor-in-chief suspects automated policing software may have acted without proper human review. Critics say the removals distort the historical record, obscure Planck’s views on quantum mechanics, and raise concerns about vanished papers by less famous scientists. (CIDRAP)
Critics Warn New ACIP Charter Could Restrict Vaccine Access: CIDRAP reports that critics see Health and Human Services Secretary Robert F. Kennedy Jr.’s revised charter for the Advisory Committee on Immunization Practices as a way to further entrench his vaccine-policy overhaul. Kennedy had promised not to alter ACIP, yet later dismissed its 17 members, installed appointees criticized as underqualified, and narrowed the childhood vaccine schedule before a federal judge paused the changes. The new charter broadens ACIP’s mission from vaccine recommendations to other disease-prevention approaches and loosens member expertise requirements. Public-health experts warn this could justify fewer vaccine recommendations, weaken Vaccines for Children coverage, politicize committee governance, and delay evidence-based guidance. Medical societies say the revisions emphasize data gaps in ways that could restrict access, especially for low-income children, and erode public trust nationally. (CIDRAP)
Inflammation Genes Point Toward Epigenetic Aging Targets: A new Clinical Epigenetics study uses Mendelian randomization, multi-omics mapping, spatial transcriptomics, and drug-target screening to probe why inflammation appears to accelerate biological aging. The authors screened 91 circulating inflammatory proteins against six aging phenotypes and identified IL-12B, IFNG, and IL-2 as especially consistent pro-aging mediators. Their analysis also highlighted seven high-confidence effector genes linked to epigenetic age acceleration, including NHLRC1, TPMT, SELP, RIPPLY3, ZNF373A, PLDN, and EDARADD. The chromosome 6p21 NHLRC1–TPMT locus stood out as a major methylation-driven node. The paper frames inflammaging as more than correlation, offering candidate targets for precision anti-aging interventions, though the work remains computational and will need experimental validation before therapeutic claims can be made. (Clinical Epigenetics)
Chromatin Collapse May Explain a Pediatric Cancer Paradox: Malignant rhabdoid tumor is devastating partly because it behaves aggressively despite having a relatively simple mutational profile. A new Clinical Epigenetics review argues that the answer may lie in chromatin architecture. The disease is defined by biallelic loss of SMARCB1, a key SWI/SNF chromatin-remodeling component. Without it, enhancer organization and transcriptional control are reshaped, leaving tumor cells dependent on a smaller number of essential regulatory nodes. The authors call this state “transcriptional bottleneck formation,” where survival and cell-cycle programs become concentrated around vulnerable control points rather than driven by classic oncogenic mutations. RUNX-family regulation of BIRC5 is presented as one example. The model suggests future therapies may need to disrupt tumor architecture, not just mutation-driven signaling. (Clinical Epigenetics)
Lead Exposure Alters Brain Methylation in Aged Zebrafish: Environmental Epigenetics published new work examining how lead exposure may affect the aging brain through DNA methylation. Researchers exposed two-year-old male zebrafish to different concentrations of Pb2+ for five days, then analyzed brain tissue using whole-genome bisulfite sequencing. Lead exposures at or above 100 μg/L significantly increased global methylation in the aged brain. Differentially methylated genes were mainly located in gene body regions and were associated with ion transport and signal transduction pathways. Only some methylation shifts matched changes in gene expression, but several affected genes were linked to locomotor-related functions, including shank1, ptprsa, plxna2, and aopep. The findings point to epigenetic mechanisms as possible contributors to lead-related neurobehavioral effects in older organisms. (Environmental Epigenetics)
RNA Feeding Tool Probes Daphnia DNA Methyltransferases: A new Environmental Epigenetics paper tests RNAi-by-feeding as a way to manipulate DNA methyltransferase genes in Daphnia pulex, a freshwater microcrustacean widely used to study plasticity, maternal effects, and environmental epigenetics. The researchers targeted three DNMT orthologues using bacterial feeding regimes across two Daphnia clones. Results differed sharply by genotype: one clone suffered mortality, while the other showed increased DNMT expression in most treatments, especially under the GFP vector control. Yet DNMT-targeted RNAi reduced each target relative to the control and unexpectedly produced cross-reactivity, with one DNMT knockdown lowering expression of the others. The authors suggest immune signaling or unknown DNMT biology may be involved. The work strengthens Daphnia as a tool for experimentally testing epigenetic mechanisms. (Environmental Epigenetics)
TRAIL-R2 Silencing Linked to Aggressive Breast Cancer: A new Oncotarget report highlights epigenetic silencing of TRAIL-R2, also known as DR5, in breast cancer. TRAIL-R2 helps mediate apoptosis, but its clinical role and epigenetic regulation have remained unclear. The study found that promoter hypermethylation was associated with reduced TRAIL-R2 expression and more aggressive clinicopathological features. Lower TRAIL-R2 protein expression was also linked to postmenopausal status, while higher expression showed a trend toward better overall survival, though larger studies are needed. Because DNA methylation is potentially reversible, the authors argue that reactivating TRAIL-R2 could become a therapeutic strategy, especially for improving response to apoptosis-based treatments. The findings add to the growing case that methylation-driven gene silencing can shape cancer behavior and treatment vulnerability. (Oncotarget)
Lifestyle Program Slows One Epigenetic Aging Marker: Aging reported an exploratory randomized controlled trial suggesting that a short lifestyle intervention can move at least one DNA methylation-based aging marker. Forty-eight overweight Japanese men aged 50 or older were assigned either to usual habits or a 12-week program combining dietary counseling, exercise guidance, and daily yogurt containing Bifidobacterium longum BB536. The intervention group showed a statistically significant slowing in DunedinPACE, equal to an estimated 2.2% reduction in pace of aging, while the control group showed little change. Most other epigenetic clocks did not remain significant after correction, and the sample was small and narrow. Still, the results suggest coordinated lifestyle changes may influence biological aging measures beyond simple weight loss alone. (Aging)
Maternal Blood Test Finds Autism-Linked Methylation Clues: News-Medical covered a Communications Biology study using maternal plasma cell-free DNA to look for prenatal methylation patterns associated with later autism spectrum disorder diagnosis and maternal obesity. Because fetal brain tissue is inaccessible before diagnosis, researchers are exploring whether circulating cell-free DNA, much of it placental in origin, can provide a noninvasive window into early developmental epigenomics. The study used whole-genome bisulfite sequencing to identify differentially methylated regions linked with autism outcomes and maternal obesity. The findings do not amount to a clinical screening test, and the authors frame them as early research. Still, the work suggests prenatal methylation signatures may help illuminate how genetic susceptibility, maternal metabolic status, and placental biology intersect in neurodevelopmental risk. (Medical News)
Math Model Tracks Methylation and Blood Pressure With Age: UNLV researchers developed a mathematical model to examine how the relationship between DNA methylation and blood pressure changes across adulthood. Using long-term data from roughly 1,000 participants, the team found that methylation-blood pressure associations are not fixed over time. In some cases, methylation linked to higher blood pressure in younger adults correlated with lower blood pressure as participants aged. The study, published in Clinical Epigenetics, does not prove causation, but it argues that aging-related risk signals should be studied dynamically rather than as static biomarkers. The model could be useful for other complex diseases, including dementia, where biological risk may shift over decades. The work reinforces the value of longitudinal epigenetic data for precision medicine. (UNLV)
UK Biobank Adds a Large Epigenetic Data Layer: A University of Exeter-led project will add DNA methylation data to UK Biobank, creating a major new resource for disease research. Backed by £16 million, the study will profile blood samples from 60,000 participants across more than one million genomic sites. UK Biobank already combines biological samples, genetics, imaging, lifestyle data, and long-term health records from 500,000 volunteers. Adding methylation data should help researchers examine how gene regulation interacts with environment, aging, and disease risk. The project is expected to support studies of heart disease, dementia, mental health, cancer, and aging, with possible future expansion to the full cohort. Its biggest value may be linking epigenetic signatures to real-world exposures and later clinical outcomes. (Biobanking)
Green Mediterranean Diet May Act as Epigenetic Pencil: A EurekAlert release describes a Clinical Nutrition randomized trial connecting the Green Mediterranean diet to folate metabolism, gene expression, and cardiometabolic improvements. The diet included green tea, walnuts, reduced red and processed meat, and daily Mankai, a folate-rich aquatic plant. Participants following the Green-MED diet had increased circulating folate compared with traditional Mediterranean and standard healthy-diet groups. Researchers linked those gains to one-carbon metabolism, methylation processes, insulin sensitivity, inflammatory markers, triglyceride-to-HDL ratio, and reductions in visceral and liver fat. The study also focused on MTHFR rs1801133, finding that high Mankai adherence appeared especially beneficial for TT genotype carriers. The authors describe nutrition as an “epigenetic pencil,” shaping gene activity without changing DNA sequence. (EurekAlert)