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  • 1. Moore, Steven
    et al.
    Evans, Lewis D. B.
    Andersson, Therese
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Portelius, Erik
    Smith, James
    Dias, Tatyana B.
    Saurat, Nathalie
    McGlade, Amelia
    Kirwan, Peter
    Blennow, Kaj
    Hardy, John
    Zetterberg, Henrik
    Livesey, Frederick J.
    APP Metabolism Regulates Tau Proteostasis in Human Cerebral Cortex Neurons2015In: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 11, no 5, p. 689-696Article in journal (Refereed)
    Abstract [en]

    Accumulation of A beta peptide fragments of the APP protein and neurofibrillary tangles of the microtubule-associated protein tau are the cellular hallmarks of Alzheimer's disease (AD). To investigate the relationship between APP metabolism and tau protein levels and phosphorylation, we studied human-stem-cell-derived forebrain neurons with genetic forms of AD, all of which increase the release of pathogenic A beta peptides. We identified marked increases in intracellular tau in genetic forms of AD that either mutated APP or increased its dosage, suggesting that APP metabolism is coupled to changes in tau proteostasis. Manipulating APP metabolism by beta-secretase and gamma-secretase inhibition, as well as gamma-secretase modulation, results in specific increases and decreases in tau protein levels. These data demonstrate that APP metabolism regulates tau proteostasis and suggest that the relationship between APP processing and tau is not mediated solely through extracellular A beta signaling to neurons.

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