Home > Publications Database > Annonacin, a natural lipophilic mitochondrial complex I inhibitor, increases phosphorylation of tau in the brain of FTDP-17 transgenic mice. > print

001     141674
005     20240321221010.0
024 7 _ |a 10.1016/j.expneurol.2013.12.017
|2 doi
024 7 _ |a pmid:24389273
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024 7 _ |a 0014-4886
|2 ISSN
024 7 _ |a 1090-2430
|2 ISSN
037 _ _ |a DZNE-2020-00005
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Yamada, Elizabeth S
|b 0
245 _ _ |a Annonacin, a natural lipophilic mitochondrial complex I inhibitor, increases phosphorylation of tau in the brain of FTDP-17 transgenic mice.
260 _ _ |a Orlando, Fla.
|c 2014
|b Academic Press
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2014-03-01
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Both 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.
536 _ _ |a 344 - Clinical and Health Care Research (POF3-344)
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542 _ _ |i 2014-03-01
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|u https://www.elsevier.com/tdm/userlicense/1.0/
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650 _ 7 |a Enzyme Inhibitors
|2 NLM Chemicals
650 _ 7 |a Furans
|2 NLM Chemicals
650 _ 7 |a Lactones
|2 NLM Chemicals
650 _ 7 |a MAPT protein, human
|2 NLM Chemicals
650 _ 7 |a Microtubule-Associated Proteins
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 7 |a annonacin
|0 40372ET6TM
|2 NLM Chemicals
650 _ 7 |a Tryptophan
|0 8DUH1N11BX
|2 NLM Chemicals
650 _ 7 |a Arginine
|0 94ZLA3W45F
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Arginine: genetics
|2 MeSH
650 _ 2 |a Brain: drug effects
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Dose-Response Relationship, Drug
|2 MeSH
650 _ 2 |a Enzyme Inhibitors: pharmacology
|2 MeSH
650 _ 2 |a Furans: pharmacology
|2 MeSH
650 _ 2 |a Gene Expression Regulation: drug effects
|2 MeSH
650 _ 2 |a Gene Expression Regulation: genetics
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Lactones: pharmacology
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Microglia: drug effects
|2 MeSH
650 _ 2 |a Microtubule-Associated Proteins: metabolism
|2 MeSH
650 _ 2 |a Mitochondria: genetics
|2 MeSH
650 _ 2 |a Mitochondria: metabolism
|2 MeSH
650 _ 2 |a Mortality
|2 MeSH
650 _ 2 |a Mutation: genetics
|2 MeSH
650 _ 2 |a Neurons: drug effects
|2 MeSH
650 _ 2 |a Phosphorylation: drug effects
|2 MeSH
650 _ 2 |a Phosphorylation: genetics
|2 MeSH
650 _ 2 |a Tryptophan: genetics
|2 MeSH
650 _ 2 |a tau Proteins: genetics
|2 MeSH
700 1 _ |a Respondek, Gesine
|0 P:(DE-2719)2811600
|b 1
700 1 _ |a Müssner, Stefanie
|b 2
700 1 _ |a de Andrade, Anderson
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700 1 _ |a Höllerhage, Matthias
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700 1 _ |a Depienne, Christel
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700 1 _ |a Rastetter, Agnès
|b 6
700 1 _ |a Tarze, Agathe
|b 7
700 1 _ |a Friguet, Bertrand
|b 8
700 1 _ |a Salama, Mahmoud Elhussiny Abdelhaleen
|0 P:(DE-2719)2812096
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700 1 _ |a Champy, Pierre
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700 1 _ |a Oertel, Wolfgang H
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700 1 _ |a Höglinger, Günter
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773 1 8 |a 10.1016/j.expneurol.2013.12.017
|b : Elsevier BV, 2014-03-01
|p 113-125
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|t Experimental Neurology
|v 253
|y 2014
|x 0014-4886
773 _ _ |a 10.1016/j.expneurol.2013.12.017
|g Vol. 253, p. 113 - 125
|0 PERI:(DE-600)1466932-8
|p 113-125
|t Experimental neurology
|v 253
|y 2014
|x 0014-4886
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