As Alzheimer's disease sweeps through the brain, do the brain's immune cells sit idly by and let it happen? Or could they overreact and make the disease worse? Perhaps they call in immune cells from other parts of the body for reinforcement? These were just a few of the questions researchers grappled with at "Neuroinflammation in Diseases of the Central Nervous System," a Keystone meeting held January 25-30 in Taos, New Mexico. Read Alzforum's seven-part series to learn about the research showcased in talks, posters, and conversations at this energetically charged meeting in the high desert.
A staggeringly complex picture of neuroinflammation emerged as researchers sought to classify the myriad cellular responses that occur in the midst of neurodegenerative diseases or other forms of brain injury (see Part 1). Macrophages in the brain, including microglia, stole the show, and researchers presented data highlighting how the cells behave differently depending on their origins (see Part 2), the type of disease they're fighting, and where in the brain they reside (see Part 3). Researchers differed over how TREM2, a major risk factor for Alzheimer's and other neurodegenerative diseases, affects immune function in the brain, but agreed upon the idea that the receptor played a key role in clustering immune cells around amyloid plaques (see Part 4).
The perennial question of whether inflammation is good or bad for the brain was exemplified by data suggesting that turning down anti-inflammatory responses triggered the clearance of plaques from the brain (see Part 5). Researchers even moved beyond the brain and presented early findings suggesting that turning down systemic inflammation may slow the progression of neurodegenerative disease (see Part 6). Finally, researchers revealed that the brain's microglia are more than just trash collectors; they prune delicate synapses and may do so overzealously in the early stages of AD (see Part 7).
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