Microglia , CX3CR1and Alzheimer's Disease Pathogenesis
Dr. Bruce Lamb and colleagues examined the roles played by a protein, called CX3CR1, in two mouse models of Alzheimer's disease. Specifically, the researchers looked at whether CX3CR1: 1) activates microglia (a type of immune cell); 2) interferes with nerve cell function or promotes death; and/or 3) plays a part in beta-amyloid protein deposits or disease-associated changes to tau protein. These researchers discovered that CX3CR1 deficiency leads to reduced beta-amyloid deposits and an activation of microglia. It was determined that removing CX3CR1from microglia increased the removal of Aß. In addition, these researchers observed that CX3CR1 deficiency leads to disease-associated changes to tau protein. Taken together, these results suggest that CX3CR1 may be a potential therapeutic target for Alzheimer's disease.
Lee, S., Varvel, N.H., Konerth, M.E., Xu, G., Cardona, A.E., Ransohoff, R.M., and B.T. Lamb. CX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimer's disease mouse models. Am. J. Pathol., 177:2549-2562, 2010 (Cover article).
Bhaskar, K., Konerth, M.E., Kokiko-Cochran, O.N., Cardona, A.E., Ransohoff, R.M., and B.T. Lamb. Regulation of tau pathology by the microglial fractakine receptor. Neuron, 68:19-31, 2010.
First published on: June 10, 2008
Last modified on: August 30, 2011