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Cells Use ‘Bioelectricity’ To Coordinate and Make Group Decisions

According to the new results, as epithelial tissue grows, cells are packed more tightly together, which increases the electrical current flowing through each cell’s membrane. A weak, old, or energy-starved cell will struggle to compensate, triggering a response that sends water rushing out of the cell, shriveling it up and marking it for death. In this way, electricity acts like a health checkup for the tissue and guides the pruning process.

“This is a very interesting discovery — finding that bioelectricity is the earliest event during this cell-extrusion process,” said the geneticist GuangJun Zhang of Purdue University, who studies bioelectrical signals in zebra fish development and wasn’t involved in the study. “It’s a good example of how a widening electronic-signaling perspective can be used in fundamental biology.”

The new discovery adds to the growing assortment of bioelectrical phenomena that scientists have discovered playing out beyond the nervous system, from bacteria swapping signals within a biofilm to cells following electric fields during embryonic development. Electricity increasingly appears to be one of biology’s go-to tools for coordinating and exchanging information between all kinds of cells.

Collision-induced ribosome degradation driven by ribosome competition and translational perturbations

How cells eliminate inefficient ribosomes.

Inside every cell, ribosomes act as tiny but vital factories that build proteins, translating genetic information into the molecules that sustain life. Although ribosomes share the same basic structure, not all of them work with equal precision. Until now, scientists did not fully understand how cells detect and handle ribosomes that underperform.

Addressing this question, a team of researchers has identified a quality control mechanism that ensures only the most competent ribosomes survive. Their study, published in Nature Communications shows that ribosomes compete during protein synthesis. When translation is disrupted, the less efficient ribosomes are selectively broken down, while the stronger ones continue functioning.

Using biochemical and genetic analyses in yeast, the researchers examined how ribosomes behave when translation is disrupted. The team engineered cells to contain a functional but suboptimal ribosome variant. These slower-moving ribosomes are overtaken on messenger RNA by faster, native ribosomes, causing the two types to collide. Such ribosome-ribosome collisions activate a ubiquitination-dependent quality control pathway that selectively removes the less efficient ribosomes.

The team also explored how external factors, such as the anticancer drug cisplatin affect this process. Cisplatin, known for binding to RNA and DNA, was found to increase ribosome collisions, which in turn promoted ribosome degradation. This insight could improve understanding of how the drug acts inside cells and why it sometimes causes side effects.

The implications of this discovery extend beyond basic biology. By showing how cells maintain the quality of their protein factories, the study provides a foundation for understanding disorders caused by ribosome malfunction, known as ribosomopathies. It may also open the door to new approaches for improving the safety and effectiveness of certain drugs.

Johns Hopkins Scientists Identify Key Brain Protein That May Slow Alzheimer’s

Researchers at Johns Hopkins Medicine report that findings from a new study funded by the National Institutes of Health are helping to identify a promising new biological target for Alzheimer’s disease. The focus is a protein that produces a crucial gas within the brain.

Studies in genetically engineered mice show that the protein Cystathionine γ-lyase, also known as CSE, plays an essential role in forming memories, says Bindu Paul, M.S., Ph.D., an associate professor of pharmacology, psychiatry and neuroscience at the Johns Hopkins University School of Medicine who led the research. CSE is best known for generating hydrogen sulfide, the gas responsible for the smell of rotten eggs, but the new findings highlight its importance in brain function.

Mapping gene disruptions in sporadic early onset Alzheimer’s disease across key brain regions

A new study led by researchers at UTHealth Houston investigated both gene expression and regulation at single cell levels to reveal disruptions in gene function in three brain regions of patients with sporadic early onset Alzheimer’s disease.

The findings are published in Science Advances.

Only about 5% to 10% of patients with Alzheimer’s disease are younger than 65. Of those patients, 10% have mutations in the APP, PSEN1, and PSEN2 genes, which are associated with Alzheimer’s disease. The other 90% of these cases are classified as sporadic early onset Alzheimer’s, a rare and aggressive form of the disease that begins before age 65. The genetic tie in early onset Alzheimer’s is largely unidentified, representing a significant but understudied population.

Blood metabolite signature offers improved prediction of type 2 diabetes risk

Diabetes, a metabolic disease, is on the rise worldwide, and over 90% of cases are type 2 diabetes, where the body does not effectively respond to insulin.

Researchers from Mass General Brigham and Albert Einstein College of Medicine have identified metabolites (small molecules found in blood generated through metabolism) associated with the risk of developing type 2 diabetes in the future, and have revealed genetic and lifestyle factors that may influence these metabolites. They also developed a metabolomic signature that predicts future risk of type 2 diabetes beyond traditional risk factors.

Their results are published in Nature Medicine.

Lifespan‐Extending Endogenous Metabolites

Endogenous metabolites are small molecules produced by an organism’s own metabolism. They encompass a wide range of molecules, such as amino acids, lipids, nucleotides, and sugars, which are pivotal for cellular function and organismal health (Baker and Rutter 2023). Beyond serving as biosynthetic precursors and energy substrates, many metabolites also function as dynamic modulators of signaling and gene regulatory networks by engaging in protein–metabolite interactions, allosteric regulation, and by serving as substrates for chromatin and other post-translational modifications (Boon et al. 2020 ; Hornisch and Piazza 2025). Metabolites can function as extracellular signals activating G protein-coupled receptors (GPCRs), such as free fatty acid receptors for fatty acids, GPR81 for lactate, SUCNR1 for succinate, and TGR5 for bile acids (Tonack et al. 2013). These GPCRs are expressed in gut, adipose tissue, endocrine glands, and immune cells, linking nutrient and metabolite levels to diverse physiological responses (Tonack et al. 2013). Other metabolites serve as enzyme cofactors or epigenetic regulators. For example, methyl donors like betaine provide methyl groups for DNA and histone methylation and also act as osmolytes to protect cells under stress (Lever and Slow 2010). Some metabolites even form specialized structural assemblies. For instance, guanine crystals can form structural color in feline eyes and contribute to enhanced night vision (Aizen et al. 2018).

Perturbations of endogenous metabolite levels or fluxes have been linked to genomic instability, metabolic dysfunction, and age-related diseases, motivating study of metabolites as both biomarkers and functional modulators of aging (Adav and Wang 2021 ; Tomar and Erber 2023 ; Xiao et al. 2025). Metabolomic studies reveal characteristic metabolite changes in diabetes, cardiovascular disease, and Alzheimer’s disease (AD) (Panyard et al. 2022), suggesting that metabolites not only reflect organismal state but also can actively influence aging pathways. In subsequent sections, we will examine specific endogenous metabolites implicated in longevity regulation.

Japanese scientists just built human brain circuits in the lab

To assess how this interaction affected development, the team compared gene expression in the cortical region of the assembloid with that of a standalone cortical organoid. The cortical tissue connected to the thalamus showed signs of greater maturity, indicating that thalamus cortex communication promotes cortical growth and development.

Thalamic Signals Drive Neural Synchrony

The scientists also examined how signals traveled through the assembloid. They found that neural activity spread from the thalamus into the cortex in wave like patterns, creating synchronized activity across cortical networks.

Two wrongs make a right: How two damaging disease variants can restore health

Scientists at Pacific Northwest Research Institute (PNRI) have overturned a long-held belief in genetics: that inheriting two harmful variants of the same gene always worsens disease. Instead, the team found that in many cases, two harmful variants can actually restore normal protein function.

Their work appears in the Proceedings of the National Academy of Sciences.

Scientists report new immune insights and targets into LRRK2 mutations in Parkinson’s disease

Parkinson’s disease (PD) is a debilitating and progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra, a brain region essential for motor control. Clinically, it is marked by tremor, rigidity, bradykinesia and postural instability, symptoms that progressively erode independence and quality of life.

PD affects millions of people worldwide, including nearly one million individuals in the United States, making it one of the fastest-growing neurological disorders. In the U.S. alone, the disease imposes a profound health care and socioeconomic burden, with annual costs reaching tens of billions of dollars due to medical care, lost productivity and long-term disability.

While environmental factors contribute to disease risk, genetic drivers are increasingly recognized, with mutations in the leucine-rich repeat kinase 2 (LRRK2) gene representing one of the most common causes of both familial and sporadic PD. Understanding how LRRK2 mutations drive disease is therefore central to developing therapies that go beyond symptoms control.

The Insane Future of Mind Uploading [Documentary]

This video explores aliens, mind uploading to other species, genetic engineering, and future robots.

SOURCES:
https://en.wikipedia.org/wiki/Eagle_eye#:~https://www.scientificamerican.com/ar… • https://en.wikipedia.org/wiki/Human_c… ___ 💡 Future Business Tech explores the future of technology and the world. Examples of topics I cover include: • Artificial Intelligence & Robotics • Virtual and Augmented Reality • Brain-Computer Interfaces • Transhumanism • Genetic Engineering SUBSCRIBE: https://bit.ly/3geLDGO ___ This video explores the future of ChatGPT and 10 ways it could change society. Other related terms: aliens, alien species, advanced civilization, genetic engineering, robot, mind upload, mind uploading, brain computer interface, artificial intelligence, ai, future business tech, future technology, future technologies, etc. ℹ️ Some links are affiliate links. They cost you nothing extra but help support the channel so I can create more videos like this. #alien #aliens #avatar #avatar2 #geneticengineering #braincomputerinterface.
https://vcahospitals.com/know-your-pe
https://www.scientificamerican.com/ar
https://en.wikipedia.org/wiki/Human_c

💡 Future Business Tech explores the future of technology and the world.

Examples of topics I cover include:
• Artificial Intelligence & Robotics.
• Virtual and Augmented Reality.
• Brain-Computer Interfaces.
• Transhumanism.
• Genetic Engineering.

SUBSCRIBE: https://bit.ly/3geLDGO

This video explores the future of ChatGPT and 10 ways it could change society. Other related terms: aliens, alien species, advanced civilization, genetic engineering, robot, mind upload, mind uploading, brain computer interface, artificial intelligence, ai, future business tech, future technology, future technologies, etc.

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