PARP9 exacerbates apoptosis and neuroinflammation via the PI3K pathway in the thalamus and hippocampus and cognitive decline after cortical infarction.

A similar trend was observed in the ipsilateral hippocampal CA3 region, where the AAV-siPARP9 group showed a trend toward reduced total microglia (p > 0.05) and pro-inflammatory microglia counts (p < 0.05), with an increase in anti-inflammatory microglia (p < 0.05), while the AAV-PARP9 group exhibited an increase in total microglia (p < 0.05) and anti-inflammatory microglia (p < 0.05), with no significant change in pro-inflammatory microglia compared to the control groups (Supplementary Figure S9A, B).

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During the probe trial, these rats crossed the platform location fewer times and spent less time in the target quadrant, although the reduction in target quadrant time did not reach statistical significance (p > 0.05, Fig. 7 D; Supplementary Figure S10A).

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Our study found that while overexpression of PARP9 exacerbated neuronal apoptosis and neuroinflammation after cerebral cortical infarction, some effects were statistically significant, whereas others showed a nonsignificant trend.

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