Brain's immune cells trigger hidden damage after mini-strokes, study finds
Researchers discovered that brief, symptom-free strokes cause lasting cognitive problems by triggering excessive immune activity in the brain—and that blocking a specific receptor can prevent it. The finding could reshape how doctors treat mini-strokes, a condition that currently has no preventive therapy and affects millions annually.
Originaltitel: Blocking microglial reactivity via purinergic receptors prevents subacute cognitive deficits after TIA
Our research presents a new animal model of transient ischemic attack (TIA) that mimics brief episodes without cell loss, but results in neuronal and behavioral deficits. We identified excessive microglial reactivity, driven by acute ATP release, as a key factor in post-TIA neurological deficits, which were ameliorated by inhibiting the P2Y12 receptor, a microglia-specific purinergic receptor in the brain parenchyma responsible for activity-dependent microglial cell-cell interactions. This finding suggests that modulation of microglial reactivity offers a promising strategy to prevent cognitive impairment in TIA patients, opening avenues for future research in this underexplored area.