Amyloid-β oligomer-induced neurotoxicity by exosomal interactions between neuron and microglia.

A hallmark of Alzheimer's disease (AD) is amyloid-β (Aβ) plaque deposition in the brain, causing deficits in cognitive function. Amyloid-beta oligomers (AβOs), the soluble precursor peptides producing Aβ plaques, also produce neurotoxicity and microgliosis together with glycolytic reprogramming. Recently, monocarboxylate transporter 1 (MCT1), a key glycolysis regulator, and its ancillary protein, CD147, are found to play an important role in the secretion of exosomes, 30-200 nm vesicles in size, which are considered as toxic molecule carriers in AD.

Sp1 site is crucial for the mouse claudin-19 gene expression in the kidney cells.

Members of the claudin family play important roles in the formation of tight junctions in the kidneys, liver and intestine. Claudin-19 (Cldn19), a newly identified member of this family, is highly expressed in the kidney of the mouse. To have a better understanding on mouse claudin-19 gene expression, a 0.