Studies by a research team at Washington University School of Medicine in St. Louis indicate that a brain protein known as YKL-40 may link Alzheimerâs disease with dysfunction in circadian rhythms, suggesting that treatments that target the protein could slow the course of the disease. Their work, reported in Science Translational Medicine, found that YKL-40 is both regulated by clock genes and involved in clearing away the potentially toxic build-up of Alzheimer’s proteins in the brain. The teamâs studies indicated that Alzheimer’s patients who carry a genetic variant that reduces YKL-40 levels maintain their cognitive faculties longer than those individuals without the variant.