Research Roundup: Stanford researchers advance treatments for blindness, memory loss and respiratory disease

The Science & Technology desk gathers a weekly digest of impactful and interesting research publications and developments at Stanford. Read the latest in this week’s Research Roundup.

Stanford researchers develop retinal implant that restores reading ability in blind patients

A microchip smaller than a fingernail, surgically placed beneath the retina, has restored the ability to read in patients who lost their sight to dry age-related macular degeneration, the most common form of incurable blindness in older adults. The microchip operates alongside augmented-reality glasses equipped with a camera that captures images and projects them as infrared light onto the implant’s 378 photovoltaic pixels. 

The device, called PRIMA, was developed by Stanford ophthalmology professor Daniel Palanker and works by converting infrared light into an electrical current that stimulates surviving retinal neurons, which then relay signals to the brain.

“It’s basically like solar panels,” Palanker said to Stanford Magazine. “Every pixel is a little solar panel in the eye.”

In a clinical trial which took place in Europe, 27 of 32 patients who completed one year of follow-up regained the ability to read letters, numbers and words. 

The results were published in the New England Journal of Medicine in Oct. 2025. Science Corporation, which now manufactures PRIMA, expects European regulatory approval by summer, with U.S. Food and Drug Administration approval pending. Currently, Palanker’s lab is developing a next-generation chip with more than 10,000 pixels to further improve image resolution and enable potential facial recognition.

Stanford study finds gut bacteria drive age-related memory loss, and the decline may be reversible

Shifts in the gut microbiome that occur naturally with aging impair communication between the intestines and the brain to drive cognitive decline, but restoring that pathway can reverse memory loss, according to a mouse study from Stanford Medicine and the Arc Institute published in Nature. 

Researchers found that as mice age, their gut microbiome shifts to favor a bacterium called Parabacteroides goldsteinii, which raises levels of medium-chain fatty acids. This triggers an inflammatory response in gut immune cells, which then disrupts signaling along the vagus nerve (the communication highway between the gut) and the hippocampus (the brain region responsible for memory). 

When researchers stimulated the vagus nerve in old mice, the animals performed as well as young mice on memory and maze tasks. 

“The degree of reversibility of age-related cognitive decline in the animals just by altering gut-brain communication was a surprise,” said Christoph Thaiss, assistant professor of pathology and senior author of the study, according to Stanford Medicine. “We tend to think of memory decline as a brain-intrinsic process.”

Vagus nerve stimulation is already FDA-approved for depression and epilepsy. Researchers are now investigating whether the same gut-brain pathway exists in humans, and whether non-invasive interventions targeting gut microbiome composition could slow or reverse cognitive decline.

Stanford researchers develop nasal vaccine that protects against viruses, bacteria and allergens

In a study published in Science, Stanford Medicine researchers developed a nasal spray vaccine that protects mice against a wide range of respiratory threats, including multiple coronaviruses, common bacterial infections and house dust mite allergens. 

The vaccine differs from existing vaccines, which train the immune system to recognize specific features of a pathogen. Instead, it mimics the chemical signals that T cells use to keep the innate immune system activated in the lungs for weeks to months.

“It’s becoming increasingly clear that many pathogens are able to quickly mutate,” Bali Pulendran, the study’s senior author and a professor of microbiology and immunology, said to Stanford Medicine. “Like the proverbial leopard that changes its spots, a virus can change the antigens on its surface.”

In vaccinated mice, the innate immune response reduced viral load in the lungs by 700-fold, and any virus that broke through was met with a fully activated adaptive response within three days, compared to two weeks in unvaccinated mice. Pulendran estimates a human version could be available within five to seven years.

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