Inflammatory cues may trigger the build-up of amyloid-β protein plaques in the brains of people with Alzheimer’s disease, suggests a study published in this week’s Nature. Understanding this classic disease hallmark could help efforts to develop new therapies for this neurodegenerative disorder.
In people with Alzheimer’s disease, aggregates of amyloid-β protein build up in the brain to form plaques, leading to cell damage and memory loss. Inflammation is thought to have a role, but the exact nature of its involvement has been hard to pin down. Michael Heneka and colleagues now show in mice that inflammatory cues trigger central-nervous-system-dwelling immune cells called microglia to release specks of a protein called ASC, which binds to the amyloid-β protein and promotes the aggregation of amyloid-β clusters in the brain. This may also occur in the very early stages of Alzheimer’s disease, the authors speculate.
Using an antibody to prevent ASC from binding to amyloid-β, they show that it reduces the formation of amyloid-like aggregates in mouse studies both in cultured cells and in live animals. Prospective trials of Alzheimer’s therapies have all failed thus far, so this finding is welcome, as it suggests therapies targeting this mechanism could be clinically useful.
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