Preeclampsia is the leading cause of maternal and perinatal morbidity and mortality; however, its etiopathogenesis remains unclear, highlighting the need for new conceptual approaches to the study of this complication. In this article preeclampsia is considered as a systemic proteinopathy of the second half of pregnancy, a consequence of a neurogenic, neuroimmune, complement-mediated conflict between the mother and the fetus, associated with the production of barrier-crossing neuron-specific proteins in the fetal brain during the critical period of neurocorticogenesis after 22–24 weeks of gestation.

The aim of this review is to highlight the role of tau protein, particularly its pathological, toxic cis conformation (cis P-tau), in the cascade of pathophysiological changes in preeclampsia, taking into account the structural and functional characteristics of tau protein and the mechanisms of its pathological transformation, systemic spread leading to the formation of cistauosis, impairment of the autophagy process, and the use of tau protein as a target for diagnostic and therapeutic interventions.

Conclusion. The concept presented here describes preeclampsia as a unique multisystem ‘tautopathy’ of perinatal period, based on a neuroimmune conflict mediated by the neuron-specific proteins of the fetal brain, with a key role played by tau protein, which determines the severity and organ-specificity of preeclampsia clinical picture. This explains the temporal progression of preeclampsia and the diversity of its manifestations, and opens up entirely new directions for the development of pathogenetically based methods of diagnosis and treatment.