First-of-its-kind preventive phage therapy provides promising results against Salmonella
The mammalian gut microbiome teems with a delicate balance of bacteria and the viruses that keep them in check, called bacteriophages, or phages. Each bacterial species usually has its own set of phage partners.
When bad bacteria enter this ecosystem, there are typically no phages present, allowing them to cause mayhem. By the time the host is sick, it is too late for phages; they'll simply reach a balance with the bad bacteria.

But what if the phages in the gut could prepare for the orally ingested pathogen and strike it down as it enters the gut, negating the need for a battle?
Researchers recently demonstrated that this prophylactic approach, using an engineered, nonpathogenic E. coli bacterium, successfully protected mice from an oral Salmonella infection.

Engineered nonpathogenic E. coli produced a modified Salmonella-specific lytic phage in the gut, creating high local phage densities before pathogen exposure. Prophylactic administration protected mice from oral Salmonella infection by enabling phage amplification and bacterial lysis.

Bacteriophages, or phages, are viruses of bacteria and do not infect humans or animals. Phage therapy, the use of phages to treat bacterial infections, is particularly hard to make successful for treating intestinal pathogens.

It's challenging, especially in the gut, because phages and bacteria tend to coexist for long periods of time.

This coexistence makes establishing the high phage-to-bacteria ratio needed to treat intestinal infections hard to achieve.

That's extremely challenging to achieve in your gut.
And then once you have a bacterial infection in your gut, a lot of times it's just not even accessible to phages. It's already hidden away in the mucosa or cells of your body; it's not just free-flowing to where the phages would be able to access the bacteria.
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To work around these impediments, the team engineered a nonpathogenic E. coli bacterium to carry a phage that only infects Salmonella. This ensures that when the phage is produced, it can specifically target the pathogen.

Usually, this type of Salmonella phage remains dormant in the Salmonella bacterial genome, but researchers of this study made several genetic modifications so that it is carried by E. coli, and, once it is released into the gut, it automatically kills Salmonella in a process called lysis. This process rapidly increases the number of phages to fight the bacteria. The researchers coined this new type of phage-bacterial combination a "lytic phage-producing lysogen," or "lyto-lysogen."
Salmonella can typically detect phage DNA produced by non-Salmonella bacteria and prevent it from replicating. But in this case, the researchers were able to disguise the phage.
They were able to trick the Salmonella bacteria into thinking the phage from E. coli was 'not foreign' by adding a Salmonella gene into the E. coli genome.
A phage that comes from their E. coli can infect Salmonella, can propagate easily in Salmonella, lyse it, and then all the phages that are produced from Salmonella can just keep replicating."

This rapid reproduction eventually leads to the eradication of the infection from the gut.
What happens is that this good bacterium, the E. coli, produces all this antipathogen phage, and there is now a protective lining so that when Salmonella comes in, just after passing through the stomach and at its weakest point, it meets this high, killer density of phages.
The researchers say they targeted Salmonella due to its high global disease burden, as it can kill the elderly, children and those with HIV; it has a high prevalence of antibiotic resistance; and it has been upgraded to a high-priority pathogen.

Nature Microbiology (2026). DOI: 10.1038/s41564-026-02484-3

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'Momnesia' is real—scientists find a biological explanation for temporary forgetfulness during pregnancy

Many women say the same thing during pregnancy: They walk into a room and forget why, misplace their keys or struggle to follow a conversation. This phenomenon, often called "pregnancy brain" or "momnesia," has long lacked a clear biological explanation.
Now, a new study by researchers at Baylor College of Medicine and collaborating institutions, published in Science Bulletin, identifies a specific brain circuit in an animal model that becomes disrupted under the sustained high estrogen levels present during pregnancy. The findings offer the first biological explanation of how exposure to high levels of circulating estrogen can temporarily impair memory.
The new findings suggest a possible explanation—it may not simply be a matter of "more estrogen is better" or "worse," but rather where in the brain estrogen acts and at what levels.

"Low-level, cyclical estrogen exposure appears to support cognitive function, which is part of why hormone therapy can help postmenopausal women.
But sustained, high-level estrogen exposure seems to engage a different pathway altogether, one centered in the hypothalamus rather than the hippocampus itself. That distinction may help reconcile a lot of conflicting data in the field.
Sustained high estrogen impaired task-specific memory in mice by reducing estrogen receptor-α signaling in lateral hypothalamic GABAergic neurons, increasing activity in a hypothalamus–hippocampus circuit. Silencing this pathway prevented impairment. In pregnant women, late-pregnancy memory deficits correlated with estrogen levels and appeared temporary.
To determine whether these findings translate to humans, the researchers assessed memory performance in women across different stages of pregnancy. They found task-specific memory impairments that emerged during late pregnancy and correlated with circulating estrogen levels, even after accounting for other factors that might influence cognition. These human data support the idea that the hormone-driven circuit identified in mice may underlie the memory changes many pregnant women experience.
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Momnesia is real, it has a defined biological basis and is temporary. The memory changes observed in both mice and women were temporary and task-specific, not a sign of broader cognitive decline.

Xin Li et al, High-level estrogen impairs memory via estrogen receptor signaling in a hypothalamic–hippocampal neural circuit, Science Bulletin (2026). DOI: 10.1016/j.scib.2026.08.057