Microglia are innate immune cells of the central nervous system, involved in maintaining neural function as well as in chasing down pathogens and clearing molecular waste. Here, researchers show that some microglia play an important part in maintaining the microvasculature of the brain. Of note, capillary networks throughout the body decline in density with age, reducing the supply of nutrients and oxygen. This is particularly consequential in energy-hungry tissues such as muscles and the brain. It is known that microglia become increasingly inflammatory and senescent with advancing age; it is interesting to speculate on the degree to which this may contribute directly to the decline in vascular function in the brain.
Scientists have known that microglia play many important roles in the brain. For example, the cells police the natural blood-brain barrier that protects the organ from harmful germs in the bloodstream. Microglia also facilitate the formation of the brain's complex network of blood vessels during development. And they are known to be important in many diseases. In Alzheimer's disease, for example, recent work suggests that the loss of the immune cells is thought to increase harmful plaque buildup in the brain.
Scientists have been unsure, however, what role microglia play in maintaining blood vessels in a normal, healthy brain. The new research reveals that the cells are critical support staff, tending the vessels and even regulating blood flow. The researchers identified microglia associating with the brain's capillaries, determined what the immune cells do there and revealed what controls those interactions. Among the cells' important responsibilities is helping to regulate the diameter of the capillaries and possibly restricting or increasing blood flow as needed.
"We are currently expanding this research into an Alzheimer's disease context in rodents to investigate whether the novel phenomenon is altered in mouse models of the disease and determine whether we could target the mechanisms we uncovered to improve known deficits in blood flow in such a mouse model of Alzheimer's. Our hope is that these findings in the lab could translate into new therapies in the clinic that would improve outcomes for patients."