Increasing brain protein O-GlcNAc-ylation mitigates breathing defects and mortality of Tau.P301L mice

The microtubule associated protein tau causes primary and secondary tauopathies by unknown molecular mechanisms. Post-translational O-GlcNAc-ylation of brain proteins was demonstrated here to be beneficial for Tau.P301L mice by pharmacological inhibition of O-GlcNAc-ase. Chronic treatment of ageing...

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Veröffentlicht in:	PloS one 2013-12, Vol.8 (12), p.e84442-e84442
Hauptverfasser:	Borghgraef, Peter, Menuet, Clément, Theunis, Clara, Louis, Justin V, Devijver, Herman, Maurin, Hervé, Smet-Nocca, Caroline, Lippens, Guy, Hilaire, Gerard, Gijsen, Harrie, Moechars, Dieder, Van Leuven, Fred
Format:	Artikel
Sprache:	eng
Schlagworte:	Aging Alzheimer's disease Alzheimers disease Analysis of Variance Animals beta-N-Acetylhexosaminidases - antagonists & inhibitors Biochemistry Biochemistry, Molecular Biology Blotting, Western Brain Brain - metabolism Brain research Breathing Defects Digital music Female Genetics Health aspects Immunohistochemistry Immunoprecipitation Inhibition Kinases Life Sciences Mice Mice, Transgenic Molecular modelling Mortality Nerve Tissue Proteins - metabolism Neurodegeneration Neurodegenerative diseases Neurosciences Pharmacology Phosphorylation Physiology Plethysmography Post-translation Proteins Pyrans - chemical synthesis Pyrans - pharmacology R&D Research & development Respiration Respiratory Mechanics - drug effects Respiratory Mechanics - physiology Respiratory tract Rodents Survival Tau protein tau Proteins - genetics Tauopathies - drug therapy Tauopathies - physiopathology Thiazoles - chemical synthesis Thiazoles - pharmacology Transgenic animals
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