The fields of neuroscience and immunology melded into one at “Neuroinflammation in Diseases of the Central Nervous System,” a Keystone Symposium held January 25-30 in Taos, New Mexico. The behavior of myeloid cells in the brain drew close scrutiny at the conference, as researchers grappled with fundamental questions such as, what do microglia actually do, and how do they respond to and influence the course of neurodegenerative disease? Novel genomic and proteomic tools emerged that may help answer these questions. Researchers abandoned the old M1/M2 microglial phenotypes calling for more relevant characterizations, and embraced TREM2 and other molecules that play central roles in microglial responses. Read Jessica Shugart’s stories on the meeting’s highlights.
Researchers explored how the brain’s immune cells influence disease, and how cells and signals from outside the brain pitch in.
Researchers at a recent Keystone symposium compared the properties of microglia with those of other macrophages in the body. The cells acquire their unique personalities through both their origins and their present environment.
Researchers at Keystone attempted to distinguish microglia from other macrophages in the body, both in form and function, and monitor the way each behaves during disease.
At Keystone, scientists reported that TREM2 may promote the survival of cells surrounding plaques, but where these cells come from and what they do is still up for grabs.
Two studies suggest that the anti-inflammatory interleukin-10 prevents efficient plaque clearance and worsens AD-like pathology in mice.
Researchers at a Keystone meeting proposed that quelling inflammation outside the brain could slow the progression of Alzheimer’s and other neurodegenerative diseases.
Researchers at a Keystone meeting reported that a combination of protective and destructive signals target microglia to prune synapses in the brain. These signals may be altered during disease.