According to a new study out of UC Irvine researchers found that immune cells that normally help us fight off various infections may also fight off AD. Study results appeared in the February 16, 2016 online issue of the Proceedings of the National Academy of Sciences.
Microglia, immune cells that dwell in the brain, attempt to clear sticky amyloid plaques. However in AD, the effort is an uphill battle. Many studies have looked at the role microglia plays in AD, but very few researchers have explored whether another set of immune cells called T-cells and B-cells that live outside the brain could play a part in autoimmune diseases that might also affect AD.
To test this theory Mathew Blurton-Jones, assistant professor of neurobiology and behavior, and doctoral student Samuel Marsh bred genetically modified mice to develop AD. While this is common in animal research, their mice lacked three key immune cell types, T-cells, B-cells and NK-cells.
During autopsy they compared the immune-deficient mice brains to other mice bred to develop AD, but with intact immune systems. They found a better than twofold increase in beta-amyloid accumulation in the mice lacking the three significant immune cell types. Furthermore they found that AD mice with the intact immune systems that harbored antibodies, which are made by B-cells, accumulated in the brain, showing an association with microglia that resulted in improving beta-amyloid clearance.
To further confirm the value of this relationship between immune cells in the blood and those in the brain, the researchers transplanted healthy bone marrow stem cells into the immune-deficient Alzheimer's mice. Since T-, B- and NK-cells develop from bone marrow stem cells, this transplantation led to a reconstitution of the missing immune cells. This allowed the B-cells to produce antibodies that once again reached the brain and aided microglia in eliminating the beta-amyloid.