Background: Neurofibrillary tangles formed by hyperphosphorylated tau aggregates in the brain are one of the classical hallmarks of Alzheimer's Disease (AD). Tau aggregates have been shown to elicit cytotoxicity, leading to overall neuronal loss and cognitive decline in AD. These aggregates can be transmitted from neurons and glial cells to other brain cells through a process known as tau spreading, and ultimately reach the endothelial cells (ECs) lining the vessel walls, thus, causing dysfunction of the neurovascular unit (NVU), a complex multicellular system surrounding brain vessels.
View Article and Find Full Text PDFMitochondrial respiratory chain supercomplexes (RCS), particularly, the respirasome, which contains complexes I, III, and IV, have been suggested to participate in facilitating electron transport, reducing the production of reactive oxygen species (ROS), and maintaining the structural integrity of individual electron transport chain (ETC) complexes. Disassembly of the RCS has been observed in Barth syndrome, neurodegenerative and cardiovascular diseases, diabetes mellitus, and aging. However, the physiological role of RCS in high energy-demanding tissues such as the heart remains unknown.
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