Researchers from the Faculty of Natural Sciences at Chemnitz University of Technology have discovered fat molecules in natural collagen fibrils, the main component of connective tissue. Their research, published in Soft Matter, shows how fats affect the mechanical properties and water content of collagen fibrils.
Collagen fibrils are the basic building blocks of skin, tendons, ligaments, and bones. They hold our bodies together. Fats and oils have long been used to soften and protect leather, which consists of collagen molecules. However, it is not known how many fat molecules are contained in natural collagen fibrils.
Knowing the precise chemical composition of collagen fibrils is important for understanding biochemical processes involved in tissue growth, aging, and disease. In chemistry, the various molecular components are usually separated to study the properties of pure substances. However, biological systems contain thousands of different chemical molecules, all of which are likely important.
Scientists at Leipzig University have identified a little-known receptor, GPR133, as a key player in bone health. By stimulating this receptor with a new compound called AP503, they were able to boost bone strength in mice, even reversing osteoporosis-like conditions. The breakthrough highlights a promising path toward safer and more effective treatments for millions struggling with bone loss, while also hinting at broader benefits for aging populations.
Like bees breathing life into gardens, providing pollen and making flowers blossom, little cellular machines called mitochondria breathe life into our bodies, buzzing with energy as they produce the fuel that powers each of our cells. Maintaining mitochondrial metabolism requires input from many molecules and proteins—some of which have yet to be discovered.
Salk Institute researchers are taking a closer look at whether mitochondria rely on microproteins—small proteins that have been difficult to find and, consequently, underestimated for their role in health and disease. In their new study, a microprotein discovered just last year at Salk, called SLC35A4-MP, was found to play a critical role in upholding mitochondrial structure and regulating metabolic stress in mouse fat cells. The findings plant the seed for future microprotein-based treatments for obesity, aging, and other mitochondrial disorders.
The study, published in Science Advances on August 29, 2025, is part of a series of recent discoveries at Salk that showcase the functional importance of microproteins in cellular biology, metabolism, and stress.
In fact, they age “ten times faster in space than on the ground,” said Dr. Catriona Jamieson, the director of the Sanford Stem Cell Institute at the University of California, San Diego, a lead author of the study.
Stem cells are special cells that can develop into various kinds of tissue. Stem cell aging is potentially worrisome because it diminishes the body’s natural ability to repair its tissues and organs, potentially leading to chronic, age-related conditions like cancer, neurodegenerative diseases and heart problems.
Aging, the key risk factor for cognitive decline, impacts the brain in a region-specific manner, with microglia among the most affected cell types. However, it remains unclear whether this is intrinsically mediated or driven by age-related changes in neighboring cells. Here, we describe a scalable, genetically modifiable system for in vivo heterochronic myeloid cell replacement. We find reconstituted myeloid cells adopt region-specific transcriptional, morphological and tiling profiles characteristic of resident microglia. Young donor cells in aged brains rapidly acquired aging phenotypes, particularly in the cerebellum, while old cells in young brains adopted youthful profiles. We identified STAT1-mediated signaling as one axis controlling microglia aging, as STAT1-loss prevented aging trajectories in reconstituted cells. Spatial transcriptomics combined with cell ablation models identified rare natural killer cells as necessary drivers of interferon signaling in aged microglia. These findings establish the local environment, rather than cell-autonomous programming, as a primary driver of microglia aging phenotypes.
Claire Gizowski, Galina Popova, Heather Shin, Wendy Craft, Wenjun Kong, Bernd J Wranik, Yuheng C Fu, Tzuhua D Lin, Baby Martin-McNulty, Po-Han Tai, Kayla Leung, Nicole Fong, Devyani Jogran, Agnieszka Wendorff, David Hendrickson, Astrid Gillich, Andy Chang, Oliver Hahn are current or former employees of Calico Life Sciences LLC. The remaining authors declare no competing interest.
Edward Chang is a neurosurgeon, scientist, and a pioneering leader in functional neurosurgery and brain-computer interface technology, whose work spans the operating room, the research lab, and the engineering bench to restore speech and movement for patients who have lost these capabilities. In this episode, Edward explains the evolution of modern neurosurgery and its dramatic reduction in collateral damage, the experience of awake brain surgery, real-time mapping to protect critical functions, and the split-second decisions surgeons make. He also discusses breakthroughs in brain-computer interfaces and functional electrical stimulation systems, strategies for improving outcomes in glioblastoma, and his vision for slimmer, safer implants that could turn devastating conditions like ALS, spinal cord injury, and aggressive brain tumors into more manageable chronic illnesses.
We discuss: 0:00:00 — Intro. 0:01:17 — The evolution of neurosurgery and the shift toward minimally invasive techniques. 0:10:58 — Glioblastomas: biology, current treatments, and emerging strategies to overcome its challenges. 0:17:39 — How brain mapping has advanced from preserving function during surgery to revealing how neurons encode language and cognition. 0:24:22 — How awake brain surgery is performed. 0:29:02 — How brain redundancy and plasticity allow some regions to be safely resected, the role of the corpus callosum in epilepsy surgery, and the clinical and philosophical implications of disconnecting the hemispheres. 0:43:46 — How neural engineering may restore lost functions in neurodegenerative disease, how thought mapping varies across individuals, and how sensory decline contributes to cognitive aging. 0:54:40 — Brain–computer interfaces explained: EEG vs. ECoG vs. single-cell electrodes and their trade-offs. 1:09:02 — Edward’s clinical trial using ECoG to restore speech to a stroke patient. 1:20:41 — How a stroke patient regained speech through brain–computer interfaces: training, AI decoding, and the path to scalable technology. 1:41:10 — Using brain-computer interfaces to restore breathing, movement, and broader function in ALS patients. 1:47:56 — The 2030 outlook for brain–computer interfaces. 1:52:35 — The potential of stem cell and cell-based therapies for regenerating lost brain function. 1:57:54 — Edward’s vision for how neurosurgery and treatments for glioblastoma, Parkinson’s disease, and Alzheimer’s disease may evolve by 2040 2:00:43 — The rare but dangerous risk of vertebral artery dissections from chiropractic neck adjustments and high-velocity movements. 2:02:31 — How Harvey Cushing might view modern neurosurgery, and how the field has shifted from damage avoidance to unlocking the brain’s functions.
——- About:
The Peter Attia Drive is a deep-dive podcast focusing on maximizing longevity, and all that goes into that from physical to cognitive to emotional health. With over 90 million episodes downloaded, it features topics including exercise, nutritional biochemistry, cardiovascular disease, Alzheimer’s disease, cancer, mental health, and much more.
Peter Attia is the founder of Early Medical, a medical practice that applies the principles of Medicine 3.0 to patients with the goal of lengthening their lifespan and simultaneously improving their healthspan.
What if the end of everything came not from cosmic fate, but from us? This episode examines the physics, probability, and peril of experiments that could, in theory, unravel the universe.
