Tongji University investigators reveal that overexpressing the mitochondrial calcium uniporter (MCU) or silencing its gatekeeper MICU1 in Drosophila intestinal stem cells restores mitochondrial calcium levels, re-establishing ER–mitochondria contact sites (MERCs) via IP3R activation. This calcium oscillation-driven autophagy rejuvenates aged stem cells, rebalancing metabolic profiles and preserving gut homeostasis, highlighting a potential avenue to mitigate age-associated tissue degeneration.

Key points

• Enhancing mitochondrial Ca²⁺ uptake via MCU overexpression or MICU1 knockdown restores MitoCa²⁺ levels and reduces cytosolic Ca²⁺ overload in aged Drosophila intestinal stem cells.
• Reactivated MitoCa²⁺ triggers IP₃R-mediated ER Ca²⁺ release at MERCs, initiating Atg1/Atg13 and Class III PI3K-dependent autophagosome formation independent of AMPK.
• Restored MERC integrity and autophagy reverse DNA damage, metabolic dysregulation, and mis-differentiation, preserving gut pH homeostasis and stem cell function.

Why it matters: This discovery reveals a MERC calcium-autophagy axis as a therapeutic lever to rejuvenate aged stem cells and halt tissue decline.

A team led by CRG Barcelona deploys EPI-Clone, a targeted single-cell DNA methylation profiling method, to reconstruct clonal trajectories and quantify how blood stem cell diversity erodes with age, uncovering myeloid-biased clone expansion and its role in inflammaging.

Key points

• EPI-Clone integrates targeted single-cell CpG methylation profiling on the Tapestri platform to capture clonal barcodes across 230,358 cells.
• Aged mice and human donors exhibit up to 70% dominance of a few HSC clones, with a shift toward myeloid-biased hematopoiesis linked to inflammaging.
• Distinct CpG subsets reflect both differentiation stage and stochastic epimutations, enabling simultaneous lineage mapping and clonal barcode generation.

Why it matters: This approach enables precise tracking of HSC clonal dynamics, offering insights into inflammaging mechanisms and potential early biomarkers of age-related hematologic risk.

A team led by Coleen T. Murphy at Princeton University shows that reducing insulin receptor DAF-2 activity in C. elegans’ hypodermal tissue drives Notch ligand OSM-11 secretion, activating neuronal Notch and boosting CREB-dependent memory maintenance.

Key points

• Tissue-specific auxin-inducible degradation of DAF-2 in C. elegans hypodermis extends associative memory beyond six hours.
• Hypodermal IIS reduction upregulates the secreted Notch ligand OSM-11, which activates neuronal LIN-12/Notch signaling via LAG-1/SEL-8.
• Single-nucleus RNA-seq reveals broad upregulation of crh-1/CREB and CREB-target genes in diverse neurons, essential for memory enhancement.

Why it matters: Revealing a body-to-brain endocrine pathway opens new avenues for systemic memory modulation and potential cognitive aging therapies.

The Markusovszky University Teaching Hospital team employs machine learning to analyze pre-treatment CT-derived Hounsfield unit statistics and lung volume data, training decision trees, kernel-based classifiers, and k-nearest neighbors to predict patients at risk of radiation-induced lung fibrosis following breast radiotherapy, supporting personalized treatment planning.

Key points

• Extracted CT lung density metrics (HU mean, SD, min, max) and lung volume from planning scans.
• Trained Fine Tree, optimizable kernel, and kNN models with five-fold cross-validation on 242 breast radiotherapy cases.
• Developed a simple HPF score combining HU metrics and lung volume achieving 62.8% validation accuracy for RILI risk.

Why it matters: This approach enables proactive identification of patients at high risk for radiation-induced lung fibrosis, improving treatment personalization and reducing pulmonary toxicity.

Gov.capital outlines strategies for capitalizing on the expanding longevity economy, detailing core market drivers, key investment avenues—from biotech to wellness—and prudent risk-management techniques to build a resilient, diversified portfolio.

Key points

• Overall longevity market projected to grow from $19 B (2023) to $63 B by 2035 (CAGR 10.4%).
• Five investment pathways: core biotech, healthcare services, enablers (AI/CMO), beneficiary sectors, and diversified vehicles (ETFs, funds).
• Risks include clinical trial failures, regulatory hurdles, cash burn; mitigation via long view, diversification, and picks-and-shovels strategy.

Researchers from institutions like NIH and the Human Brain Project develop wetware systems harnessing DNA, proteins, and neural networks for computation. By engineering genetic circuits and advanced neural interfaces, they achieve direct brain-computer integration and neuromorphic processing, promising breakthroughs in neuroprosthetics, adaptive AI, and energy-efficient computing.

Key points

• Engineered DNA-based logic circuits perform parallel biochemical computations via strand hybridization and enzymatic reactions.
• Biocompatible neural interfaces transduce electrical signals from neurons into digital data streams for direct brain-computer communication.
• Neuromorphic architectures using cultured neural networks and protein logic gates mimic synaptic plasticity, achieving adaptive, energy-efficient processing.

Why it matters: Wetware computing bridges biological and digital systems, offering self-adaptive, energy-efficient AI and precise neuroprosthetic therapies beyond conventional silicon-based technologies.