Researchers at the Arc Institute, Stanford University, and NVIDIA have developed Evo 2, an advanced AI model capable of predicting genetic variations and generating genomic sequences across all domains of life.
Testing shows that Evo 2 accurately predicts the functional effects of mutations across prokaryotic and eukaryotic genomes. It also successfully annotated the woolly mammoth genome from raw genomic sequences without a direct training reference, showing an ability to generalize function from the sequence alone.
Current genomic models struggle with predicting functional impacts of mutations across diverse biological systems, particularly for eukaryotic genomes. Machine learning approaches have demonstrated some success in modeling protein sequences and prokaryotic genomes. The complexity of eukaryotic DNA, with its long-range interactions and regulatory elements, presents more of a challenge.
AI-powered precision in medicine is helping to enhance the accuracy, efficiency, and personalization of medical treatments and healthcare interventions. Machine learning models analyze vast datasets, including genetic information, disease pathways, and past clinical outcomes, to predict how drugs will interact with biological targets. This not only speeds up the identification of promising compounds but also helps eliminate ineffective or potentially harmful options early in the research process.
Researchers are also turning to AI to improve how they evaluate a drug’s effectiveness across diverse patient populations. By analyzing real-world data, including electronic health records and biomarker responses, AI can help researchers identify patterns that predict how different groups may respond to a treatment. This level of precision helps refine dosing strategies, minimize side effects, and support the development of personalized medicine where treatments are tailored to an individual’s genetic and biological profile.
AI is having a positive impact on the pharmaceutical industry helping to reshape how drugs are discovered, tested, and brought to market. From accelerating drug development and optimizing research to enhancing clinical trials and manufacturing, AI is reducing costs, improving efficiency, and ultimately delivering better treatments to patients.
Many people who have spinal cord injuries also have dramatic tales of disaster: a diving accident, a car crash, a construction site catastrophe. But Chloë Angus has quite a different story. She was home one evening in 2015 when her right foot started tingling and gradually lost sensation. She managed to drive herself to the hospital, but over the course of the next few days she lost all sensation and control of both legs. The doctors found a benign tumor inside her spinal cord that couldn’t be removed, and told her she’d never walk again. But Angus, a jet-setting fashion designer, isn’t the type to take such news lying—or sitting—down.
Ten years later, at the CES tech trade show in January, Angus was showing off her dancing moves in a powered exoskeleton from the Canadian company Human in Motion Robotics. “Getting back to walking is pretty cool after spinal cord injury, but getting back to dancing is a game changer,” she told a crowd on the expo floor.
Imagine that malignant brain tumors are not the unbridled chaos of unchecked growth we think they are, but they are actually communicating with brain cells in very specific ways. That’s what Stanford neuroscientist Michelle Monje MD, PhD, discovered about certain types of brain cancer (called gliomas), including a deadly childhood form called DIPG. It turns out that these tumors can form connections with the brain’s circuitry (just like brain cells do) in order to fuel their own growth. But it’s not just cancers that start in the brain that are doing this. Monje and Stanford researcher Julien Sage, PhD, discovered that a type of cancer that starts in the lungs also engages in this form of hijacking when it spreads to the brain. This is important because we now have significant insight into the process of tumor growth. And these findings help us better understand how we might be able to treat or stop these cancers altogether. For more information, read “Dangerous infiltrators” in Stanford Medicine magazine: https://stan.md/4gZHRh7
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A small clinical trial, published in Occupational & Environmental Medicine, suggests that melatonin supplementation may help counteract DNA
DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).
Shen et al. investigate the use of Lactobacillus plantarum, a commensal bacterial strain, as a chassis for targeting the olfactory mucosa to facilitate precise nose-to-brain delivery of therapeutic molecules. When engineered to secrete appetite-regulating hormones, intranasal delivery of L. plantarum alleviates obesity-related symptoms in a mouse model.
“Can you hand me the… you know… the thingy? It’s right there next to that other doohickey!” Struggling to find the right word happens to all of us. In fact, it even has a name; lethologica, and it tends to become more common as we get older.
Forgetting words now and then isn’t a big deal, but if it starts happening frequently, it could be an early sign of changes in the brain linked to Alzheimer’s disease —long before more obvious symptoms appear. But here’s the twist: A recent University of Toronto study suggests that how fast you speak might be a better clue about brain health than the occasional word mix-up.
Humanity came close to extinction 800,000 years ago. Only 1,280 of our ancestors survived.
A recent study published in Science suggests that a catastrophic “ancestral bottleneck” reduced the global population to just 1,280 breeding individuals, wiping out 98.7% of the early human lineage.
This population crash, lasting about 117,000 years, likely resulted from extreme climate shifts, prolonged droughts, and dwindling food sources.
Using a groundbreaking genetic analysis method called FitCoal, researchers analyzed modern human genomes to trace this dramatic decline, potentially explaining a gap in the African and Eurasian fossil record.
Despite the near-extinction, this bottleneck may have played a crucial role in shaping modern humans. Scientists believe it contributed to a key evolutionary event—chromosome fusion—which may have set Homo sapiens apart from earlier hominin species, including Neanderthals and Denisovans. The study raises intriguing questions about how this small population survived, possibly through early fire use and adaptive intelligence. Understanding this ancient crisis helps scientists piece together the story of human evolution and the resilience that allowed our species to thrive against all odds.
