Li et al. present a microLED-based mesoscale optogenetic system for centimeter-scale, million-pixel primate cortical stimulation. Optogenetically evoked saccades with accurate retinotopic organization remain stable for over a year, demonstrating precise, robust, and durable neuromodulation and charting a path toward next-generation optical brain-computer interfaces and visual prostheses.
“Despite greater white matter degeneration and reduced cortical thickness, APOE ε4 carriers exhibited preserved deep brain volumes and better self-reported well-being. This study highlights the complex interplay between genetic factors and neurodegenerative processes. Our future research aims to provide more natural history data of EPM1 and correlate long-term phenotypic data with additional geno-phenotypic analyses.”
Read this original article from Epileptic Disorders at doi.org/10.1002/epd2.70112.
Objective Progressive myoclonic epilepsy type 1 (EPM1) is a neurodegenerative disease caused by biallelic variants in the cystatin B (CSTB) gene. Despite a progressive course, phenotype severity varies among patients, even within families. We studied the potential role of APOE ε4 in modifying phenotypic diversity in EPM1, given its established association with neurodegeneration, particularly in Alzheimer’s disease.
Scientists mapped every possible mutation in a key genetic hotspot, revealing how distinct mutations drive tumor growth differently, which could influence anticancer therapy success.
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Mapping diverse mutations within a cancer hotspot revealed that distinct variants drive tumor growth to different extents, which could guide anticancer therapies.
Here, Miguel Verbitsky & team analyze urine from 325 participants in the Randomized Intervention for Children with Vesicoureteral Reflux study (RIVUR study), revealing genetic variations influence bacterial composition of urine in children with recurrent urinary infections and vesicoureteral reflux:
The image shows cytokeratin 5 and smooth muscle actin labeling after UTI in mouse bladder, which increases expression of Cxcl12 and Cxcr4.
3Department of Dermatology; and.
4Center for Precision Medicine and Genomics, Columbia University, New York, New York, USA.
5Department of Neurology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Despite the absence of a fully established regulatory framework or unified technological standard for industrial-and clinical-grade organoid biomanufacturing yet, substantial progress has been made toward building the technical and institutional infrastructure required for scalability and reproducibility. The Organisation for Economic Co-operation and Development (OECD) introduced the Good In Vitro Method Practices (GIVIMP)19, an international quality-assurance framework that defines laboratory quality systems, method qualification, reference controls, equipment calibration, and data integrity—principles that now potentially serve as quantitative benchmarks for process validation in organoid production. Complementing this, the NIH Standardized Organoid Modeling (SOM) Center was recently established to promote the development of organoid platforms that are reproducible, robust, and broadly accessible for translational biomedical and pharmaceutical research.
Expanding these standardization efforts, a recent publication introduced the Essential Guidelines for Manufacturing and Application of Organoids, delineating a systematic workflow encompassing cell sourcing, culture optimization, quality control, and biobanking logistics20. Their framework identifies organ-specific critical quality attributes (CQAs)—including growth-factor composition, morphological fidelity, and quantitative analytical metrics—and recommends standardized cryopreservation conditions (~100–200 organoids per vial) to enhance batch comparability. Likewise, a recent study established quantitative criteria for human intestinal organoid standardization, specifying cell-line provenance, minimum lineage composition thresholds (e.g., ≥30% enterocytes), and molecular marker expression profiles consistent with physiological differentiation21. Taken together, these coordinated initiatives—from international organizations to national agencies and individual laboratories—represent an emerging global framework toward reproducible, quality-controlled, and scalable organoid biomanufacturing, laying the groundwork for eventual regulatory convergence and clinical translation.
In response to these prevailing limitations and in alignment with global standardization trends, a range of engineering strategies has been developed, shifting the paradigm from organoid culture to organoid manufacturing by enabling reproducible and scalable organoid production. These strategies broadly focus on two goals: improving reproducibility by minimizing uncontrolled variation in the culture environment as well as by regulating intrinsic morphogenetic processes, and enhancing scalability by increasing productivity and throughput. To this end, recent advances can be categorized into three major domains: cellular engineering approaches that regulate morphogenetic processes through programmed cell organization; material-based strategies that establish defined and controllable environmental cues; and platform-or system-level innovations that enable high-throughput and automated workflows. Together, these innovative engineering advances mark aion toward more standardized, efficient production workflows.
The last few weeks in longevity science have been absolutely unreal. In this episode of Longevity Science News, Emmett Short breaks down 5 bombshell breakthroughs that could reshape the future of human health in 2026 — including an FDA-approved trial aiming to reverse cellular aging, cancer vaccines eliminating brain tumors in days, the regeneration of human teeth, one-shot GLP-1 Ozempic-style gene therapies, and a shocking new discovery linking gut bacteria to multiple sclerosis.
These aren’t sci-fi predictions — these are real developments happening right now in clinical trials, biotech labs, and cutting-edge medical research. If you care about anti-aging, regenerative medicine, epigenetic reprogramming, cancer immunotherapy, GLP-1 weight loss drugs, or the future of human lifespan, this is the episode you don’t want to miss.
Hume Band 20% off with Code LSN20
https://humehealth.com/pages/hume-ban… Huma Band Review: • Best Fitness Tracker For Longevity: Hume B… JOIN LSN Patreon for exclusive access to news, tips and a community of like minded longevity enthusiasts: https://www.patreon.com/user?u=29506604 ✅ Chapters 00:00 – The Longevity Science Explosion 00:48 Hume Band 20% Off 01:02 – Exclusive Interviews 01:43 Bombshell #1: FDA Approves Age Reversal Trial (Yamanaka Factors) 04:40 – Bombshell #2: Cancer’s Worst Month Ever (Vaccines + Immunotherapy) 09:19 – Bombshell #3: The Regeneration Revolution (Cartilage, Teeth, Liver) 11:30 – Bombshell #4: The One-Shot Ozempic Gene Therapy 12:25 – Bombshell #5: Gut Bacteria Linked to Multiple Sclerosis 13:55 – Final Recap + What Breakthrough Comes Next? Links in Script David Sinclair FDA Trial Tweet
https://twitter.com/davidasinclair/status/2
… FDA Greenlights Age Reset Trial (Endpoints) https://endpoints.news/exclusive-fda–… Life Biosciences Epigenetic Reprogramming Video • Reprogramming Human Life — Michael Ringel… mRNA Brain Cancer Vaccine Tweet
just setting up my twttr
— jack (@jack) March 21, 2006
… ANKTIVA Glioblastoma Case Tweet
https://twitter.com/LoriMills4CA42/status/2
… Dr. Patrick Soon-Shiong ANKTIVA Clip Tweet
stalking my coworkers
— crystal (@crystal) March 24, 2006
… Dr. Soon-Shiong Cancer Clip (YouTube) • Patrick Soon-Shiong’s cancer drug Anktiva… MIT/Stanford AbLecs Cancer Breakthrough Tweet
https://twitter.com/ShiningScience/status/2
… Universal mRNA Cancer Vaccine Tweet
https://twitter.com/ShiningScience/status/2
… AI Urine Test for Cancer Detection Tweet
https://twitter.com/Dr_Singularity/status/2
… Akkermansia Gut Bacteria + Immunotherapy Tweet
https://twitter.com/drwilliamli/status/2006
… Cartilage Regeneration Tweet (Liz Parrish)
I feel bad for Pluto. No one likes being demoted.
— David Warner (@hiddeninput) August 24, 2006
… Stanford Cartilage Regeneration Article https://news.stanford.edu/stories/202… Tooth Regrowth Drug Trial Tweet
https://twitter.com/kimmonismus/status/2006
… NewLimit Liver Rejuvenation Tweet
https://twitter.com/byersblake/status/20086
… One-Shot GLP-1 Gene Therapy Thread (Cremieux) https://twitter.com/cremieuxrecueil/status/.… MS Gut Bacteria Breakthrough Video Tweet
trying to get odeo thoughts down
— Ev (@ev) March 23, 2006
… ⚠️ Disclaimer: This video is for educational and informational purposes only and does not constitute medical advice. Consult a qualified clinician before making health or treatment decisions. 🔗 EXCLUSIVE INTERVIEWS & BONUS CONTENT Get extended conversations, deep dives, and behind-the-scenes research ans a YouTube Member Patreon: 👉 / u29506604 YT Membership: 👉
/ @longevitysciencenews PRODUCTION CREDITS ⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺⎺ Executive Producer – Keith Comito @Retromancers Host, Producer, Writer – Emmett Short @emmettshort
Full huma band review: • best fitness tracker for longevity: hume B…
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✅ Chapters.
Gas vesicles are among the largest known protein nanostructures produced and assembled inside microbial cells. These hollow, air-filled cylindrical nanostructures found in certain aquatic microbes have drawn increasing interest from scientists due to their potential for practical applications, including as part of novel diagnostic and therapeutic tools. However, producing gas vesicles is a difficult task for cells in the lab, hindering the development of applications.
In a study recently published in Nature Communications, a team of researchers led by Rice University bioengineer George Lu reports the development of a new genetic regulatory system to improve cell viability during the production of gas vesicles.
“In the past few years, studies have shown that gas vesicles’ ability to reflect sound makes them useful as unique and versatile acoustic reporter systems for biomedical research and clinical applications,” said Lu, an assistant professor in the Department of Bioengineering at Rice’s George R. Brown School of Engineering and Computing.
Euan Ashley’s lab explores the intricate interactions of gene variants. Tiny “typos,” or genetic mutations, can sneak into segments of DNA. Many of these are harmless, but some can cause health problems. Two or more genes can team up and change the outcome of a physical or molecular trait. This phenomenon, known as epistasis, occurs through complex interactions between genes that are functionally related—such as those that support protein creation.
Identifying these group dynamics provides crucial clues to how genetic diseases manifest and should be treated. But they’re not easily detected and often fly under the radar.
To help root out these connections, Ashley, MB ChB, DPhil, professor of genetics and of biomedical data science, and a team of scientists, including co-corresponding author Bin Yu, Ph.D., a professor of statistics and of electrical engineering and computer sciences at the University of California, Berkeley, have developed computational techniques to identify and understand the hidden ways epistasis influences inherited diseases.
As for decay accelerating factor (DAF); also known as CD55, it is a type I cell surface protein that forms a single chain anchored to the membrane by glycosylphosphatidylinositol (GPI). It binds C3b and C4b inhibiting thereby the formation of C3 convertase and decreasing its half-life, thus providing a protective barrier threshold for plasma membranes of normal autologous cells against complement deposition and activation9,10.
The role of the complement system in cancer is complicated and has been debated for long. Malignant transformation is generally accompanied by genetic and epigenetic modifications which drastically alter patterns of glycosylation, cell-surface proteins and phospholipids11. These alterations can be identified by innate and adaptive immune mechanisms that guard the host against cancer development12. This is the known basis of the immune surveillance hypothesis. There is no direct evidence to support the argument that complement is able to eradicate emerging tumors. Nevertheless, taking into consideration that complement is intended for the recognition of non-self-elements, it is assumed that alterations in the tumor cell membranes’ composition render these cells as targets for complement recognition13. However, the relationship between inflammation and cancer is complicated and subject to contradictory forces14. Therefore, while acute responses are considered a vital part of the defense against cancerous cells, continuous inflammation in the tumor microenvironment increases the threat of neoplastic transformation and has several tumor-promoting effects15.
The current study aims at investigating the expression levels of mCRPs; CD46 and CD55 in the acute lymphocytic leukemia and acute myelogenous leukemia and to further elucidate its role in Egyptian cancer patients. To the best of our knowledge this study is one of very few studies tackling the complicated role of the complement system in acute leukemia.