Lynx1 suppression reopens the window for effective rehabilitation after stroke in mice.

Lynx1 suppression in peri-infarct layer 5 pyramidal neurons promotes synaptic clustering and dendritic spine turnover, reopening effective rehabilitation in chronic-phase stroke mice.

• Why it matters: Rehabilitation reliably improves motor recovery after stroke, but its effectiveness drops from the subacute to chronic phase, likely reflecting reduced neural plasticity; the underlying molecular and cellular timing is unclear.
• What they did: In a focal ischemic stroke mouse model, Lynx1 was identified as a negative regulator of post-stroke neural plasticity, with longitudinal intravital imaging showing that Lynx1 suppression increased dendritic spine turnover and clustered spine formation in the peri-infarct area.
• The result: Lynx1 suppression improved spontaneous motor recovery and rehabilitation efficacy in the chronic phase, and a Lynx1-targeting antisense oligonucleotide administered during the chronic phase further enhanced rehabilitation responsiveness.

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