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001     140512
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024 7 _ |a 10.1016/j.neurobiolaging.2018.11.026
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024 7 _ |a pmid:30640040
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024 7 _ |a 0197-4580
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024 7 _ |a 1558-1497
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037 _ _ |a DZNE-2020-06834
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Pickhardt, Marcus
|0 P:(DE-2719)2810282
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245 _ _ |a Screening of a neuronal cell model of tau pathology for therapeutic compounds.
260 _ _ |a Amsterdam [u.a.]
|c 2019
|b Elsevier Science
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2019-04-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a We have developed a cell-based phenotypic automated high-content screening approach for N2a cells expressing the pro-aggregant repeat domain of tau protein (tauRDΔK), which allows analysis of a chemogenomic library of 1649 compounds for their effect on the inhibition or stimulation of intracellular tau aggregation. We identified several inhibitors and stimulators of aggregation and achieved a screening reproducibility >85% for all data. We identified 18 potential inhibitors (= 1.1% of the library) and 10 stimulators (= 0.6% of the library) of tau aggregation in this cell model of tau pathology. The results provide insights into the regulation of cellular tau aggregation and the pathways involved in this process (e.g., involving signaling via p38 mitogen-activated protein kinase, histone deacetylases, vascular endothelial growth factor, rho/ROCK). For example, inhibitors of protein kinases (e.g., p38) can reduce tau aggregation, whereas inhibitors of deacetylases (histone deacetylases) can enhance aggregation. These observations are compatible with reports that phosphorylated or acetylated tau promotes pathology.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2019-04-01
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650 _ 7 |a Enzyme Inhibitors
|2 NLM Chemicals
650 _ 7 |a Histone Deacetylase Inhibitors
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 7 |a p38 Mitogen-Activated Protein Kinases
|0 EC 2.7.11.24
|2 NLM Chemicals
650 _ 7 |a Histone Deacetylases
|0 EC 3.5.1.98
|2 NLM Chemicals
650 _ 2 |a Cell Line
|2 MeSH
650 _ 2 |a Drug Evaluation, Preclinical: methods
|2 MeSH
650 _ 2 |a Enzyme Inhibitors: pharmacology
|2 MeSH
650 _ 2 |a Histone Deacetylase Inhibitors
|2 MeSH
650 _ 2 |a Histone Deacetylases: pharmacology
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Models, Biological
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: genetics
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: metabolism
|2 MeSH
650 _ 2 |a Signal Transduction: genetics
|2 MeSH
650 _ 2 |a Signal Transduction: physiology
|2 MeSH
650 _ 2 |a Tauopathies: drug therapy
|2 MeSH
650 _ 2 |a Tauopathies: genetics
|2 MeSH
650 _ 2 |a Tauopathies: metabolism
|2 MeSH
650 _ 2 |a p38 Mitogen-Activated Protein Kinases: antagonists & inhibitors
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
700 1 _ |a Tassoni, Michele
|0 P:(DE-2719)2810678
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|u dzne
700 1 _ |a Denner, Philip
|0 P:(DE-2719)2810245
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700 1 _ |a Kurkowsky, Birgit
|0 P:(DE-2719)2810323
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700 1 _ |a Kitanovic, Ana
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700 1 _ |a Möhl, Christoph
|0 P:(DE-2719)2810422
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700 1 _ |a Fava, Eugenio
|0 P:(DE-2719)2159508
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700 1 _ |a Mandelkow, Eckhard
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773 1 8 |a 10.1016/j.neurobiolaging.2018.11.026
|b : Elsevier BV, 2019-04-01
|p 24-34
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|t Neurobiology of Aging
|v 76
|y 2019
|x 0197-4580
773 _ _ |a 10.1016/j.neurobiolaging.2018.11.026
|g Vol. 76, p. 24 - 34
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