title: Expression of tau reduces secretion of Abeta without altering the amyloid precursor protein content in CHOsw cells.
abstract: Insoluble deposits of tau and amyloid precursor protein (APP) peptides Abeta characterize Alzheimer's disease. We studied the role of tau in the metabolism of APP in cells stably expressing APP Swedish mutation (CHOsw). Transient expression of tau in CHOsw cells caused morphological changes, bundling of microtubules and perinuclear aggregation of Golgi-derived vesicles. It also reduced the secretion of Abeta(1-40) and Abeta(1-42) without altering the APP steady state levels. This was accompanied by a reduction in the gamma-secretase and an increase in the insulin degrading enzyme activities. Our results suggest that tau may play an inhibitory role in the amyloidogenic activity of APP.
authors.affiliation: Neuroinflammation Research Laboratories, Department of Psychiatry of the Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
authors.forename: Zhong
authors.initials: Z
authors.lastname: Zhao
authors.forename: Hanna
authors.initials: H
authors.lastname: Ksiezak-Reding
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Giulio Maria
authors.initials: GM
authors.lastname: Pasinetti
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D016466:CHO Cells; D006224:Cricetinae; D010766:Phosphorylation; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D016875:tau Proteins