Medical Bulletin 23/February/2026 - Video

Here are the top medical news for today:

Review Suggests Gut Microbiome Influences Response to GLP-1 Drugs

What if the reason some people lose more weight—or see better blood sugar control—on GLP-1 drugs lies in their gut bacteria? A new review published in the British Journal of Clinical Pharmacology explores the two-way relationship between glucagon-like peptide-1 receptor agonists (GLP-1RAs) and the gut microbiome, highlighting potential implications for metabolic health and personalized medicine.

More than 500 million people worldwide live with type 2 diabetes, and obesity rates continue to rise. GLP-1RAs such as liraglutide, semaglutide and dulaglutide have transformed treatment by improving insulin secretion, reducing appetite and lowering cardiovascular risk. Yet patient responses vary widely—prompting researchers to examine whether gut microbes play a role.

The review synthesizes findings from clinical and preclinical studies examining how gut bacteria regulate GLP-1 secretion and how GLP-1RAs, in turn, alter microbial composition. Gut microbes break down dietary fiber into short-chain fatty acids (SCFAs) like butyrate, acetate and propionate. These metabolites stimulate GLP-1 release from intestinal L-cells via G-protein-coupled receptors and intracellular signaling pathways. Butyrate may also enhance proglucagon gene expression, supporting sustained hormone production.

Bile acids—modified by intestinal bacteria—further regulate GLP-1 through receptors such as TGR5 and FXR, demonstrating a dynamic microbial-hormonal interaction. Conversely, dysbiosis can promote inflammation via lipopolysaccharide activation of TLR4 and NF-κB signaling, potentially impairing insulin and GLP-1 pathways.

Evidence also suggests GLP-1RAs reshape the microbiome. Studies report enrichment of beneficial species such as Akkermansia muciniphila and shifts in the Firmicutes-to-Bacteroidetes ratio, alongside reduced inflammatory markers. However, results are inconsistent, likely influenced by diet, weight loss, metformin use and study design differences.

Importantly, small pilot studies indicate that baseline microbial signatures may predict stronger HbA1c reductions. Early machine-learning models show promise in forecasting treatment response based on microbiome profiles.

While animal studies suggest microbial shifts may contribute to metabolic improvements, definitive human causal data remain limited. The authors conclude that controlled, longitudinal studies integrating diet standardization and multiomics tools are needed to clarify whether microbiome-guided therapy could enhance the precision and long-term effectiveness of GLP-1RA treatment in obesity and type 2 diabetes.

REFERENCE: Kamath S, Chan NSL, Joyce P. (2026). GLP-1 agonists and the gut microbiome: A bidirectional relationship. British Journal of Clinical Pharmacology, 1-17. DOI: 10.1002/bcp.70487, https://bpspubs.onlinelibrary.wiley.com/doi/10.1002/bcp.70487

Peripheral Retina Changes Could Signal Early Alzheimer’s, Research Finds

What if Alzheimer’s disease could be detected during a routine eye exam—years before memory loss begins? A new study suggests that early warning signs of the disease may be hiding in the far edges of the retina, not the center typically examined in standard vision tests. The research, led by scientists at Houston Methodist Hospital, was published in the Journal of Alzheimer's Disease.

Alzheimer’s disease (AD) is marked by the buildup of amyloid proteins in the brain, leading to progressive neurodegeneration. Previous studies have shown that amyloid accumulation in the retina mirrors similar deposits in the brain, suggesting the eye may reflect early disease processes. However, most clinical exams focus on the central retina, which is responsible for sharp vision. This new study shifts attention to the peripheral retina—the outer region of the eye.

Using mouse models of early-stage Alzheimer’s, researchers examined how Müller glia—specialized retinal support cells—respond during the earliest phases of disease development. They compared changes between central and peripheral retinal regions. The team found that the peripheral retina, which contains a higher density of glial cells, showed significant structural and cellular alterations before classic neurological symptoms appeared.

A key finding involved Aquaporin-4, a protein that helps clear metabolic waste—including amyloid—from the central nervous system. In early disease stages, Aquaporin-4 levels increased, particularly in the peripheral retina. This was accompanied by enlarged and more numerous glial cells, indicating cellular stress and an intensified effort to maintain tissue balance before widespread brain damage occurs.

Researchers interpret these changes as evidence that the body’s “waste-clearing” system is working harder in the earliest stages of Alzheimer’s. Because these retinal alterations appear before significant cognitive decline, they may offer a valuable window for early detection.

While the findings are based on animal models and require validation in humans, the study suggests that advanced retinal imaging focused on the periphery could one day support earlier diagnosis and monitoring of Alzheimer’s—potentially opening the door to earlier intervention and improved outcomes.

REFERENCE: Das, G., Raghunathan, R., Wang, L., Wan, Z., Vasquez, M., Zhao, H., & Wong, S. T. (2026). Retinal Müller glia alterations and their impact on ocular glymphatic clearance in an Alzheimer’s disease mouse model. Journal of Alzheimer’s Disease. https://doi.org/10.1177/13872877261418165

New Stem Cell Approach Targets Dopamine Loss in Parkinson’s Patients

What if Parkinson’s disease could be treated not just by easing symptoms—but by replacing the very cells that are lost? Scientists at Keck Medicine of USC are testing whether implanted stem cells can restore dopamine production in the brain, potentially improving movement and altering the course of the disease.

Parkinson’s disease is a progressive neurological disorder affecting more than one million people in the United States. It occurs when dopamine-producing neurons gradually die, particularly in brain regions that control movement. Dopamine is essential for coordinating smooth, controlled muscle activity. As levels decline, patients develop tremors, stiffness, slowed movements and balance problems. Current treatments—such as dopamine-replacing medications—can reduce symptoms but do not stop the underlying neurodegeneration.

In this early-phase clinical trial, researchers are implanting laboratory-engineered induced pluripotent stem cells (iPSCs) directly into the brain. Unlike embryonic stem cells, iPSCs are created by reprogramming adult cells, such as skin or blood cells, back into a flexible state. These cells are then guided in the lab to mature into dopamine-producing neurons.

During the procedure, neurosurgeons create a small opening in the skull and use MRI guidance to precisely deliver the engineered cells into the basal ganglia—the brain region responsible for movement coordination. The goal is for the transplanted cells to survive, integrate with surrounding brain tissue, and begin producing dopamine naturally.

Participants are monitored closely for 12 to 15 months after surgery to evaluate motor function improvements and assess safety. Doctors are watching for potential side effects, including dyskinesia (involuntary excessive movements), immune reactions or infection. Long-term follow-up will continue for up to five years to determine whether the therapy provides sustained benefit.

Researchers hope that restoring dopamine at its source could “jump-start” the brain’s own signaling systems. While still experimental, this regenerative approach represents a shift from symptom management toward cellular repair—offering new hope for slowing progression and improving quality of life in Parkinson’s disease.

REFERENCE: University of Southern California - Health Sciences. "Doctors implant dopamine-producing stem cells in Parkinson’s patients." ScienceDaily. ScienceDaily, 20 February 2026. .