Disabling an enzyme may improve brain artery function in aged mice
In an experiment in 18-month-old mice with a partial enzyme deficiency, disabling a second enzyme in blood-vessel lining cells improved abnormal artery responses.
Limit: The blood–brain barrier result measured protein expression rather than barrier function
Edited by Boris Djordjevic · AgingResearch.News
In an animal experiment, researchers studied 18-month-old mice partially deficient in endothelial nitric oxide synthase, an enzyme that helps blood vessels relax. They genetically disabled BACE1, a protein-cutting enzyme, specifically in cells lining blood vessels.
In mice with the partial deficiency, basilar arteries, which supply the brain, contracted instead of relaxing in response to acetylcholine, a chemical signal. They also contracted more strongly in response to another test chemical than arteries from mice without the deficiency. Disabling BACE1 reduced contractions to the second chemical and changed the acetylcholine response to moderate relaxation. It also increased production of a protein fragment described as protective for blood vessels and restored levels of claudin-5, a protein that helps seal the blood–brain barrier.
Why it matters
Understanding how blood-vessel lining cells process proteins could help identify ways to preserve brain artery function during aging.
Caveats
This genetic experiment involved aged mice with a specific enzyme deficiency, not people receiving a drug. The reported blood–brain barrier result concerned protein expression rather than a direct test of barrier function.
The paper
Mayo Clinic College of Medicine
American Journal of Physiology Heart and Circulatory Physiology, Oct 16, 2026
