Preeclampsia-induced neuroimmune alterations in offspring: glial dysregulation, apoptosis, and impaired cognition 9346

Abstract Description Preeclampsia (PreE), a hypertensive disorder during pregnancy, increases the risk of cognitive and behavioral issues in offspring. This study uses the vasopressin mouse model of PreE to examine its effects on offspring neurodevelopment and behavior. Offspring were analyzed for glial cell composition, cytokine concentrations, apoptosis, and brain-derived neurotrophic factor (BDNF). Blood-brain barrier (BBB) integrity was assessed in adult offspring, who also underwent the Plus-maze task to evaluate spatial memory. Offspring from PreE pregnancies showed reduced microglia and astrocyte populations at one week of age, with sex-specific changes by week seven. Females had increased microglia and astrocyte frequencies, while only astrocytes were elevated in males. Annexin staining was also significantly increased in PreE offspring. At 12 weeks of age, female offspring of PreE had higher BDNF levels, and BBB integrity was compromised in adult offspring of both sexes. PreE offspring also demonstrated impaired spatial memory. These findings suggest that PreE disrupts neuroimmune development, causing long-term effects on glial cells, apoptosis, neurotrophic support, and cognition. Females appear more susceptible to PreE-induced neuroinflammation and cognitive impairments, potentially mediated by altered glial activity and apoptosis. Targeting neuroimmune dysregulation and BBB dysfunction may reduce PreE’s lasting impact on offspring development. Funding Sources NIH 1K01HL155240-01 UL1TR002494 Topic Categories Neuroimmunology (NEUR)