More than 700 participants hailing from 35 countries gathered in Keystone, Colorado, June 17–21 for a joint Keystone symposium: Advances in Neurodegenerative Disease Research and Therapy; and New Frontiers in Neuroinflammation: What Happens When CNS and Periphery Meet? Researchers presented fresh findings on how microglial meddling steers neurodegeneration, on tau’s latest antics, on ApoE’s actions independent of Aβ, and how aging transmits from the blood into the brain. Participants jumped back and forth between the two side-by-side symposia, and packed poster sessions abuzz with intense discussions capped off each data-filled day. Check out Alzforum’s coverage for the highlights.
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
At Keystone, the work of several groups painted TREM2 as a dedicated supporter of microglial function across neurodegenerative disease models, including those for ALS.
At a Keystone meeting, researchers agreed that ApoE stokes damaging neuroinflammation in response to tau pathology. The E4 allele ramped up cholesterol biosynthesis in microglia and astrocytes, and even promoted neuronal damage when expressed outside of the brain.
At Keystone, researchers placed pathological tau on both sides of the synaptic cleft, along with complement proteins. Activated microglia gobbled up tau-laden neurons, and even may have facilitated tau’s spread in the brain.
Blood from an old mouse ages the brain of a young one, but how? Researchers report that VCAM1 on brain endothelial cells facilitates the process.