A compound produced in the digestive tracts of many people appears to accelerate the brain changes behind Alzheimer's disease, according to a study published in Nature Communications in August 2026.
Researchers at the University of Wisconsin-Madison tracked the compound, called imidazole propionate (ImP), in the blood of almost 1,200 adults and found that those with the highest levels showed more dementia biomarkers and faster declines on cognitive tests. In mice, the same compound worsened Alzheimer's-like damage in the brain.
The finding, reported by the university, does not prove that ImP causes Alzheimer's disease. But it points to a specific molecule researchers hope could one day be targeted with a drug, in the way statins target cholesterol to lower heart-disease risk.
What the compound is and where it comes from
Imidazole propionate is made when certain gut bacteria break down histidine, an essential amino acid found in protein-rich foods such as meat, fish, eggs and dairy. The bacteria that produce it use an enzyme called urocanate reductase, and known producers include species of Streptococcus, Lactobacillus, Clostridium and Veillonella, according to a 2024 review in Diabetes and Metabolic Syndrome.
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Elevated ImP has previously been linked to type 2 diabetes and cardiovascular disease, including higher mortality in heart failure. The new Wisconsin study is among the first to tie the same metabolite to Alzheimer's pathology.
Federico Rey, a UW-Madison professor of bacteriology and co-author of the study, said the bacteria that make ImP are common but usually a small share of the gut community. "ImP-producing bacteria are present in a large fraction of people, but they're not very abundant in most people," Rey said in the university's announcement.
Higher blood levels, faster decline
The team, led by Rey and gerontology professor Barbara Bendlin, analyzed blood samples from participants in the Wisconsin Registry for Alzheimer's Prevention and the Wisconsin Alzheimer's Disease Research Center. In the peer-reviewed paper, higher plasma ImP was associated with lower scores on preclinical cognitive tests and with elevated markers of neurodegeneration, including neurofilament light chain and phospho-tau-217.
About 43 percent of participants carried a common genetic variant that was linked to accumulating higher ImP in the blood, possibly by affecting how efficiently the kidneys clear the compound. The same genetic region has previously turned up in large genetic studies as a marker of Alzheimer's risk.
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In mice given ImP in their drinking water for months, brain tissue showed more amyloid plaques and greater tau-related damage, and the blood-brain barrier became more permeable. That work builds on earlier research from the same lab suggesting the gut microbiome can shape brain pathology, including a study in which healthy rats developed Alzheimer's-like symptoms after receiving gut bacteria transferred from patients.
Why a treatment is not around the corner
Because histidine is essential and widely present in the diet, simply cutting foods will not remove ImP from the equation. Bendlin said broad dietary improvement is a reasonable step but not a targeted answer.
"Generally improving your diet would probably help," Bendlin said. "But it's not as easy as saying, 'Stop eating eggs' or 'Don't eat so much red meat.' Because you need histidine, and it's all over the place."
The more promising avenue, the researchers say, is to design a drug that lowers ImP itself. Bendlin drew a comparison with cardiovascular medicine. "It could be just like cholesterol, where people with elevated cholesterol take a drug, a statin, that reduces their risk for heart disease," she said. "If we can find an inhibitor that can help decrease the levels of ImP in the blood, that could hopefully reduce the risk of Alzheimer's and the speed of cognitive decline for a significant number of people."
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No such drug exists yet. The findings are early, and clinical trials would need to show that lowering ImP actually changes disease outcomes in people. Anyone worried about memory changes or family history should raise those concerns with a physician rather than act on a single new study.
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This article is made and published by Jesper Bengtson, who may have used AI in the preparation.