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000141674 0247_ $$2doi$$a10.1016/j.expneurol.2013.12.017
000141674 0247_ $$2pmid$$apmid:24389273
000141674 0247_ $$2ISSN$$a0014-4886
000141674 0247_ $$2ISSN$$a1090-2430
000141674 037__ $$aDZNE-2020-00005
000141674 041__ $$aEnglish
000141674 082__ $$a610
000141674 1001_ $$aYamada, Elizabeth S$$b0
000141674 245__ $$aAnnonacin, a natural lipophilic mitochondrial complex I inhibitor, increases phosphorylation of tau in the brain of FTDP-17 transgenic mice.
000141674 260__ $$aOrlando, Fla.$$bAcademic Press$$c2014
000141674 264_1 $$2Crossref$$3print$$bElsevier BV$$c2014-03-01
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000141674 520__ $$aBoth genetic and environmental factors likely contribute to the neuropathology of tauopathies, but it remains unclear how specific genetic backgrounds affect the susceptibility towards environmental toxins. Mutations in the tau gene have been associated with familial tauopathies, while annonacin, a plant-derived mitochondrial inhibitor, has been implicated in an environmental form of tauopathy. We therefore determined whether there was a pathogenic synergy between annonacin exposure and the expression of the R406W-tau mutation in transgenic mice. We found that annonacin exposure caused an increase in the number of neurons with phosphorylated tau in the somatodendritic compartment in several brain areas in R406W(+/+) mice as opposed to mice that had only the endogenous mouse tau (R406W(-/-)). Western blot analysis demonstrated a concomitant increase in total tau protein without increase in tau mRNA, but reduced proteasomal proteolytic activity in R406W(+/+), but not R406W(-/-) mice, upon annonacin-treatment. Phosphorylated tau levels exceeded the increase in total tau protein, along with increased levels of different tau kinases, foremost a striking increase in the p25/p35 ratio, known to activate the tau kinase Cdk5. In summary, we observed a synergistic interaction between annonacin exposure and the presence of the R406W-tau mutation, which resulted in reduced degradation, increased phosphorylation and redistribution of neuronal tau.
000141674 536__ $$0G:(DE-HGF)POF3-344$$a344 - Clinical and Health Care Research (POF3-344)$$cPOF3-344$$fPOF III$$x0
000141674 542__ $$2Crossref$$i2014-03-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
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000141674 650_7 $$2NLM Chemicals$$aEnzyme Inhibitors
000141674 650_7 $$2NLM Chemicals$$aFurans
000141674 650_7 $$2NLM Chemicals$$aLactones
000141674 650_7 $$2NLM Chemicals$$aMAPT protein, human
000141674 650_7 $$2NLM Chemicals$$aMicrotubule-Associated Proteins
000141674 650_7 $$2NLM Chemicals$$atau Proteins
000141674 650_7 $$040372ET6TM$$2NLM Chemicals$$aannonacin
000141674 650_7 $$08DUH1N11BX$$2NLM Chemicals$$aTryptophan
000141674 650_7 $$094ZLA3W45F$$2NLM Chemicals$$aArginine
000141674 650_2 $$2MeSH$$aAnimals
000141674 650_2 $$2MeSH$$aArginine: genetics
000141674 650_2 $$2MeSH$$aBrain: drug effects
000141674 650_2 $$2MeSH$$aBrain: metabolism
000141674 650_2 $$2MeSH$$aDose-Response Relationship, Drug
000141674 650_2 $$2MeSH$$aEnzyme Inhibitors: pharmacology
000141674 650_2 $$2MeSH$$aFurans: pharmacology
000141674 650_2 $$2MeSH$$aGene Expression Regulation: drug effects
000141674 650_2 $$2MeSH$$aGene Expression Regulation: genetics
000141674 650_2 $$2MeSH$$aHumans
000141674 650_2 $$2MeSH$$aLactones: pharmacology
000141674 650_2 $$2MeSH$$aMice
000141674 650_2 $$2MeSH$$aMice, Inbred C57BL
000141674 650_2 $$2MeSH$$aMice, Transgenic
000141674 650_2 $$2MeSH$$aMicroglia: drug effects
000141674 650_2 $$2MeSH$$aMicrotubule-Associated Proteins: metabolism
000141674 650_2 $$2MeSH$$aMitochondria: genetics
000141674 650_2 $$2MeSH$$aMitochondria: metabolism
000141674 650_2 $$2MeSH$$aMortality
000141674 650_2 $$2MeSH$$aMutation: genetics
000141674 650_2 $$2MeSH$$aNeurons: drug effects
000141674 650_2 $$2MeSH$$aPhosphorylation: drug effects
000141674 650_2 $$2MeSH$$aPhosphorylation: genetics
000141674 650_2 $$2MeSH$$aTryptophan: genetics
000141674 650_2 $$2MeSH$$atau Proteins: genetics
000141674 7001_ $$0P:(DE-2719)2811600$$aRespondek, Gesine$$b1
000141674 7001_ $$aMüssner, Stefanie$$b2
000141674 7001_ $$0P:(DE-2719)2813101$$ade Andrade, Anderson$$b3
000141674 7001_ $$0P:(DE-2719)2813308$$aHöllerhage, Matthias$$b4
000141674 7001_ $$aDepienne, Christel$$b5
000141674 7001_ $$aRastetter, Agnès$$b6
000141674 7001_ $$aTarze, Agathe$$b7
000141674 7001_ $$aFriguet, Bertrand$$b8
000141674 7001_ $$0P:(DE-2719)2812096$$aSalama, Mahmoud Elhussiny Abdelhaleen$$b9
000141674 7001_ $$aChampy, Pierre$$b10
000141674 7001_ $$0P:(DE-2719)9000908$$aOertel, Wolfgang H$$b11
000141674 7001_ $$0P:(DE-2719)2811373$$aHöglinger, Günter$$b12$$eLast author
000141674 77318 $$2Crossref$$3journal-article$$a10.1016/j.expneurol.2013.12.017$$b : Elsevier BV, 2014-03-01$$p113-125$$tExperimental Neurology$$v253$$x0014-4886$$y2014
000141674 773__ $$0PERI:(DE-600)1466932-8$$a10.1016/j.expneurol.2013.12.017$$gVol. 253, p. 113 - 125$$p113-125$$tExperimental neurology$$v253$$x0014-4886$$y2014
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