RESUMEN
PURPOSE OF REVIEW: We reviewed a wide body of emerging research highlighting the possibility for premenstrual exacerbations of mood symptoms in polycystic ovary syndrome (PCOS). RECENT FINDINGS: Neuroendocrine dysregulation, sensitivity to ovarian hormone fluctuations as well as higher levels and types of adverse childhood experiences and demographic factors are emerging factors explaining high rates of psychiatric disorders in PCOS. Ovulatory dysfunction, common in PCOS, significantly interferes with one's identity and quality of life. Results on pharmacologic and non-pharmacologic treatments for mood symptoms are mixed, though improvements in the physical sequalae of PCOS could also improve mood symptoms. However, significant improvements on the methodological quality are needed, particularly the evaluation of mood symptoms across the menstrual cycle. Evidence is preliminary on whether there are premenstrual exacerbations of psychiatric symptoms in PCOS. Prospective, longitudinal studies with larger sample sizes are needed to comprehensively understand the psychiatric profile in PCOS.
RESUMEN
Microglia, the resident immune cells of the central nervous system, are intimately involved in the brain's most basic processes, from pruning neural synapses during development to preventing excessive neuronal activity throughout life. Studies have reported both helpful and harmful roles for microglia at the blood-brain barrier (BBB) in the context of disease. However, less is known about microglia-endothelial cell interactions in the healthy brain. To investigate the role of microglia at a healthy BBB, we used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia and analyzed the BBB ultrastructure, permeability, and transcriptome. Interestingly, we found that, despite their direct contact with endothelial cells, microglia are not necessary for the maintenance of BBB structure, function, or gene expression in the healthy brain. However, we found that PLX5622 treatment alters brain endothelial cholesterol metabolism. This effect was independent from microglial depletion, suggesting that PLX5622 has off-target effects on brain vasculature.