Preeclampsia history and postpartum risk of cerebrovascular disease and cognitive impairment: Potential mechanisms.

Hypertensive disorders of pregnancy such as preeclampsia, eclampsia, superimposed preeclampsia, and gestational hypertension are major causes of fetal and maternal morbidity and mortality. Women with a history of hypertensive pregnancy disorders have increased risk of stroke and cognitive impairments later in life. Moreover, women with a history of preeclampsia have increased risk of mortality from diseases including stroke, Alzheimer's disease, and cardiovascular disease. The underlying pathophysiological mechanisms are currently not fully known. Here, we present clinical, epidemiological, and preclinical studies focused on evaluating the long-term cerebrovascular and cognitive dysfunction that affect women with a history of hypertensive pregnancy disorders and discuss potential underlying pathophysiological mechanisms.

Pial Vessel-Associated Microglia/Macrophages Increase in Female Dahl-SS/Jr Rats Independent of Pregnancy History.

As the resident immune cells of the central nervous system, microglia have a wide range of functions such as surveillance, phagocytosis, and signaling through production of chemokines and cytokines. Recent studies have identified and characterized macrophages residing at the meninges, a series of layers surrounding the brain and spinal cord. While perivascular microglia within the brain parenchyma increase following chronic hypertension, there are no reports of changes at the meninges, and specifically, associated with the pial vasculature. Thus, we used female Sprague Dawley and Dahl salt-sensitive (SS/Jr) rat brains, stained for ionized calcium-binding adapter molecule (Iba1), and characterized microglia/macrophages associated with pial vessels in the posterior brain. Results indicate that Iba1+ pial vessel-associated microglia (PVAM) completely surrounded the vessels in brains from the Dahl-SS/Jr rats. PVAM density was significantly higher and distance between PVAMs lower in Dahl-SS/Jr compared to the Sprague Dawley rat brains. Pregnancy history did not affect these findings. While the functional role of these cells are not known, we contextualize our novel findings with that of other studies assessing or characterizing myeloid cells at the borders of the CNS (meninges and choroid plexus) and perivascular macrophages and propose their possible origin in the Dahl-SS/Jr model of chronic hypertension.