Alzheimer's plaque may be the brain's antimicrobial defense

Researchers at Massachusetts General Hospital and Harvard Medical School tested a different idea in mouse brains and in human neural cells grown in a dish: that the sticky protein might first be doing a job.

In 5XFAD mice, which make human amyloid-beta, herpes simplex virus in the brain rapidly seeded plaque, and the mice survived the infection better than normal littermates. In 3D cultures of human neural cells, herpes simplex and two forms of human herpesvirus 6 seeded amyloid deposits within 48 hours.

The team's reading is that amyloid-beta functions as part of the brain's innate immune system, seeded rapidly wherever a pathogen appears, with Alzheimer's disease representing that defense running chronically out of control. The idea reframes decades of failed anti-amyloid drugs and points toward infection as a trigger worth studying, though the mouse and dish findings have not been shown to explain human disease directly.

Plaque may be a trap, not just wreckage.