Alzheimer’s Amyloid Gets Immune System Trim

Immune cells in the brain have a trigger, and when it is pulled, it prompts immune cells to degrade toxic β-amyloid (Aβ) proteins.This new finding, from Sanford Burnham Prebys Medical Research Institute (SBP), helps explain why a faulty trigger appears to raise the risk of Alzheimer’s disease.
Increasing the genetic expression of the trigger—a way of pulling the trigger more often—could prevent or reduce the severity of Alzheimer’s disease and other neurodegenerative disorders.
“We could use brain immune cells to solve what’s becoming a public health crisis.” “These studies are important because they show that in addition to rescuing the pathology associated with Alzheimer’s disease, we are able to reduce the behavioral deficits with TREM2,” added Dr. Xu. “To our knowledge, this provides convincing evidence that minimizing Aβ levels alleviates Alzheimer’s disease symptoms.” As they learn more about how TREM2 modulates the amyloid signals that put microglia to work, the Xu lab and other researchers have their work cut out for them.
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