by National Institute on Aging
Scientists only recently discovered lymphatic vessels in the brain that remove cellular debris and other waste. Now, new NIA-supported research published in Nature on July 25 suggests these vessels could play a role in age-related cognitive decline and Alzheimer’s disease.
Researchers from the University of Virginia, Charlottesville, studied the performance of lymphatic vessels in the brains of mice and the drainage of cerebral spinal fluid (CSF) from blood vessels into the lymph nodes—also known as the brain’s waste-removal system.
Using methods that impaired the function of the lymphatic vessels in younger mice resulted in decreased drainage of large molecules from CSF into lymph nodes, reduced flow of CSF in certain areas of the brain involved in learning and memory, and reduced spatial learning and memory abilities.
Researchers compared the function of lymphatic vessels in younger and older mice. They found that in older mice, lymphatic vessels were narrower, and large molecules did not drain out of the CSF into the lymph nodes as well. Using a method to boost lymphatic function in older mice resulted in improved cognitive function.
Researchers also found that impairing brain lymphatic vessels in mouse models of Alzheimer’s disease led to higher levels of amyloid-beta deposits in the tissue covering the brain as the mice aged. Abnormal buildup of the protein amyloid-beta is a factor in Alzheimer’s disease. The researchers’ findings in the mouse models were mirrored in postmortem analysis on the brains of nine people who had Alzheimer’s disease.
According to the researchers, determining whether altering lymphatic vessels in people would have similar benefit to what was seen in the mouse models requires further study, but these initials findings could point to a new possible target for preventing or delaying age-related cognitive decline and Alzheimer’s disease.
Reference: Da Mesquita S, et al. Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease. Nature. 2018 Jul 25. doi: 10.1038/s41586-018-0368-8. [Epub ahead of print].