Exploring the Mechanism of Postpartum Cognitive Dysfunction in a Preeclampsia Rat Model via Multimodal Imaging

Preeclampsia (PE) affects 3%-5% of pregnancies worldwide and is a leading cause of maternal/perinatal mortality, yet its etiology remains unknown. We established a PE rat model using L-NAME to investigate postpartum cognitive dysfunction and its mechanisms, evaluated brain microstructural changes with MRI, explored correlations between MRI parameters and cognitive impairment, and assessed pravastatin's therapeutic effects. Sixty-three pregnant rats were divided into normal pregnant (NP), PE, and pravastatin-treated (PRA) groups, with three postpartum subgroups (10 days, 1 month, 3 months; n = 7 each). Morris water maze, HE/Nissl staining, transmission electron microscopy, and multimodal MRI (DTI, IVIM, DCE-MRI) were performed. ROIs included anterior/posterior cortex and hippocampus. Pearson correlation was used to relate MRI parameters to escape latency. (1) L-NAME induced a PE-like phenotype, alleviated by pravastatin. (2) Cognitive impairment appeared at 10 days postpartum and worsened over time. (3) FA, D, and f values decreased while Ktrans increased in the PE group (p < 0.05), changes that progressed over time and were abrogated by pravastatin. (4) FA and D were negatively correlated with escape latency, whereas Ktrans showed a positive correlation. (5) Neuronal degeneration, astrocyte activation, and BBB disruption in the PE group were ameliorated by pravastatin. PE model rats developed progressive postpartum cognitive dysfunction, likely due to neuronal degeneration, glial activation, and increased BBB permeability. Pravastatin partially alleviated these pathological and cognitive changes. Multimodal MRI effectively detected alterations in brain microstructure, microvascular perfusion, and BBB, consistent with histopathological findings.