Medical Bulletin 24/December/2025 - Video

Here are the top medical news for today:

Study finds fatty diets reprogram liver cells, raising cancer risk

Every meal you eat could be quietly shaping your liver’s future. A new study from the Massachusetts Institute of Technology (MIT), published in Cell, reveals how a high fat diet can rewire liver cells, pushing them back into an immature, stem cell like state that helps them survive stress—but at a dangerous cost. Over time, these “reverted” cells become far more likely to turn cancerous, explaining why fatty diets are among the strongest risk factors for liver cancer worldwide.

Liver cancer often develops after years of fat buildup and inflammation, a condition known as steatotic liver disease. While this disease is usually linked to obesity, alcohol, or metabolic disorders, the molecular steps connecting diet and cancer have remained unclear. To fill that gap, scientists from MIT’s Koch Institute for Integrative Cancer Research and Harvard MIT Program in Health Sciences and Technology tracked how the liver changes under the stress of a fatty diet.

Using single cell RNA sequencing, the team analyzed liver cells from mice fed a high fat diet over time. This powerful method allowed them to measure which genes were switched on or off as liver inflammation progressed to scarring and, ultimately, cancer. Early in the disease process, hepatocytes—the liver’s main functional cells—began switching on genes that promote survival and proliferation, while silencing those responsible for normal metabolism. “It’s a trade off,” explained lead author Constantine Tzouanas. “The cells protect themselves from stress, but in doing so, they lose their mature identity—making them more vulnerable to tumor causing mutations.”

By the study’s end, nearly all mice on the high fat diet had developed liver tumors. The researchers also pinpointed key transcription factors—including SOX4 and thyroid hormone receptor—that control this regression process.

When the team examined human liver samples, they saw the same pattern: declining function in mature liver genes and rising expression of “pro survival” ones predicted poorer patient outcomes after cancer developed.

The next step, researchers say, is to test whether returning to a balanced diet or using emerging weight loss drugs like GLP 1 agonists can reverse these molecular changes before irreversible damage occurs.

This discovery offers fresh hope that by targeting early cellular reprogramming, doctors may one day prevent liver cancer in those most at risk—starting not in the tumor, but in the dinner plate.

REFERENCE: Tzouanas, Constantine N. et al.; Hepatic adaptation to chronic metabolic stress primes tumorigenesis; Cell, Volume 0, Issue 0; DOI: 10.1016/j.cell.2025.11.031

Scientists uncover brain mechanisms underlying schizophrenia and bipolar disorder

Mental illnesses like schizophrenia and bipolar disorder remain some of medicine’s biggest mysteries—difficult to diagnose and even harder to treat. Now, for the first time, scientists have grown miniature brain organoids in the lab to uncover how neurons behave differently in these disorders. The study, published in APL Bioengineering by researchers at Johns Hopkins University, reveals distinct electrical patterns in brain tissue derived from patients with schizophrenia or bipolar disorder, offering a possible step toward more accurate diagnosis and personalized treatment.

Both schizophrenia and bipolar disorder disrupt thought and emotion, but their underlying biology has remained elusive because no single brain region or enzyme can pinpoint the problem. To bridge this gap, lead researcher Dr. Annie Kathuria, a biomedical engineer at Johns Hopkins, and her team turned to brain organoids—pea sized clusters of neurons grown from a patient’s blood or skin cells that mimic the structure and function of the developing human brain.

Using induced pluripotent stem cells (iPSCs) from twelve participants—some with schizophrenia, some with bipolar disorder, and healthy controls—the researchers cultured organoids representing the prefrontal cortex, the brain’s decision making hub. They placed these organoids on microchips fitted with multi electrode arrays, enabling them to record tiny bursts of electrical activity, much like a miniature EEG. Then, they applied machine learning algorithms to decode patterns that distinguished diseased organoids from healthy ones.

The models identified unique neural “signatures” for each disorder, including differences in firing rates, rhythmic timing, and spike distribution. Remarkably, the system was able to correctly identify whether an organoid came from a healthy or diseased individual with 83 percent accuracy—a figure that rose to 92 percent after mild electrical stimulation revealed hidden neural dynamics.

These findings mark a potential turning point in psychiatry. By expanding this work, clinicians might one day test new medications directly on patient derived organoids, optimizing drug doses without trial and error.

As the team collaborates with neurosurgeons and psychiatrists to analyze more samples, their next goal is equally ambitious: using these lab-grown “mini brains” to predict which drugs-and at what concentrations-will restore healthy neural activity, moving psychiatry closer to a future of personalized, biology based mental healthcare.

REFERENCE: “Machine learning-enabled detection of electrophysiological signatures in iPSC-derived models of schizophrenia and bipolar disorder” by Kai Cheng, Autumn Williams, Anannya Kshirsagar, Sai Kulkarni, Rakesh Karmacharya, Deok-Ho Kim, Sridevi V. Sarma and Annie Kathuria, 22 September 2025, APL Bioengineering; DOI: 10.1063/5.0250559

Breakthrough in Parkinson’s research reshapes understanding of dopamine’s role

For decades, dopamine has been thought of as the brain’s “go” signal—a chemical that controls how fast or strong our movements are. But a new study from McGill University, published in Nature Neuroscience, is rewriting that understanding. Researchers found that dopamine doesn’t directly dictate movement speed or force. Instead, it acts more like engine oil that keeps the system running smoothly, providing the necessary conditions for movement to occur at all.

This discovery challenges long standing views of dopamine’s role in neurological disorders like Parkinson’s disease, a condition that affects more than 110,000 Canadians and millions worldwide. Parkinson’s develops when dopamine producing neurons in the brain gradually die, leading to symptoms such as tremors, slowed motion, and stiffness. Treatments like levodopa, which boosts dopamine levels, often restore mobility—but scientists have never fully understood why it works so effectively.

To answer that question, a team led by Dr. Nicolas Tritsch, assistant professor in McGill’s Department of Psychiatry and researcher at the Douglas Research Centre, turned to advanced mouse studies. Using optogenetics, a technique that uses light to control specific brain cells, the researchers monitored motor behavior while precisely turning dopamine neurons “on” or “off.” Mice were trained to press a weighted lever—a task requiring both speed and strength—while their brain activity was recorded in real time.

If brief dopamine bursts truly controlled movement intensity, changing dopamine levels mid task should have altered how hard or fast the animals pushed. Yet no such changes occurred. Instead, the researchers found that boosting dopamine beforehand helped the mice initiate movement but did not affect how forcefully they moved once they began. Conversely, restoring dopamine with levodopa improved overall ability to move, not moment by moment motion control.

The findings could reshape how Parkinson’s therapies are designed. Instead of targeting quick dopamine spikes, future treatments may focus on maintaining stable baseline dopamine levels—a simpler and potentially safer approach. By reframing dopamine as an essential enabler, rather than a micromanager, neuroscientists hope to refine treatment strategies that help patients reclaim motion and independence.

REFERENCE: Haixin Liu, Riccardo Melani, Marta Maltese, James Taniguchi, Akhila Sankaramanchi, Ruoheng Zeng, Jenna R. Martin, Nicolas X. Tritsch. Subsecond dopamine fluctuations do not specify the vigor of ongoing actions. Nature Neuroscience, 2025; 28 (12): 2432 DOI: 10.1038/s41593-025-02102-1