Imidazole propionate, a compound made by gut bacteria, increased amyloid and tau buildup in mice and tracked with worse cognition in Alzheimer's patients, opening a research stage path aimed at blood, not brain.
Gut bacteria make a compound called imidazole propionate, or ImP, that has joined the short list of blood-measurable Alzheimer's targets. New mouse and human data suggest lowering it could become a way to slow the disease.
The amount of ImP a person makes varies sharply, and the bacteria that produce it live in many people without dominating anyone's gut. Once ImP enters the bloodstream it can reach the brain. A Nature Communications paper from University of Wisconsin-Madison researchers Barbara Bendlin, Federico Rey and their colleagues reports that in mice, ImP reaching the brain increased the abnormal beta-amyloid and tau buildups that drive Alzheimer's. Eventually those buildups kill neurons, the disease's defining feature in humans.
In people, higher ImP tracked with worse cognition among participants already in the Alzheimer's group, ScienceDaily reports. Earlier work from the same lab had tied ImP to type 2 diabetes and coronary artery disease, published in 2017. A UW-Madison release notes the group had also shown the gut microbial mix differs between people with Alzheimer's and healthy controls.
This is not a treatment. The research-stage move is to lower ImP in the blood, an intervention aimed at the gut rather than the brain. A recent review lays out the open questions any human ImP-reduction trial would have to answer first.