This technology uses EPA protein or a synthetic portion of EPA protein to promote the degradation and clearance of Tau in neurons and to prevent neurodegeneration and the development or progression of Alzheimer’s disease (AD). Studies have shown that the reduction of Tau levels in neurons attenuates neuronal dysfunction in mouse model of AD and the extent of Tau accumulation correlates with cognitive decline in human patients. This novel AD treatment approach is supported by in vitro and in vivo data. In vitro co-immunoprecipitation experiments have shown that this EPA interacts with Tau. In vitro co-expression experiments have shown that only a specific isoform of this EPA reduces the levels of Tau. Transfection studies have shown that the overexpression of this same EPA isoform reduces the levels of intracellular Tau in human neuronal cells. Knockout studies have shown that this EPA isoform is required for long term survival of neuronal cells, the inactivation of this EPA isoform increases Tau levels in neuronal cells and that the accumulation of Tau in neuronal cells promotes neurodegeneration. Benoît Doré benoit.dore@axelys.ca (514) 340 8521
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Get ready to take your space management game to the next level with the University of Glasgow’s innovative project! By combining the