Home > Publications Database > Tau neurotoxicity and rescue in animal models of human Tauopathies. > print

001     138382
005     20240321220426.0
024 7 _ |a 10.1016/j.conb.2015.09.004
|2 doi
024 7 _ |a pmid:26431808
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024 7 _ |a 0959-4388
|2 ISSN
024 7 _ |a 1873-6882
|2 ISSN
024 7 _ |a altmetric:4584583
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037 _ _ |a DZNE-2020-04704
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Krüger, Lars
|0 P:(DE-2719)2810335
|b 0
|e First author
245 _ _ |a Tau neurotoxicity and rescue in animal models of human Tauopathies.
260 _ _ |a Philadelphia, Pa.
|c 2016
|b Current Biology
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2016-02-01
336 7 _ |a article
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336 7 _ |a Journal Article
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|x Review Article
336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Pathological Tau is a hallmark of various neuronal disorders and spreads in the brain of Alzheimer patients in a well-defined manner. Beside Tau's main function in stabilizing microtubules for axonal transport, a variety of novel functions for neurons and glia have emerged recently. Tau regulates the susceptibility to hyperexcitation and plays a role in neuron-glia contact formation. Studies implicate soluble oligomeric species of Tau, rather than insoluble aggregates, as more detrimental to proper neuronal function. Tau is not exclusively intracellular; instead Tau can be released into the extracellular space. This has led to the hypothesis of a prion-disease like mechanism to explain the stereotypical progression of Tau. Targeting pathological Tau with antibodies or aggregation inhibitors may help to prevent pathology.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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|f POF III
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542 _ _ |i 2016-02-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Antibodies
|2 NLM Chemicals
650 _ 7 |a Protein Aggregates
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Antibodies: pharmacology
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Brain: physiopathology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Disease Susceptibility
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Presynaptic Terminals: metabolism
|2 MeSH
650 _ 2 |a Protein Aggregates: drug effects
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: metabolism
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: physiopathology
|2 MeSH
650 _ 2 |a Tauopathies: metabolism
|2 MeSH
650 _ 2 |a Tauopathies: physiopathology
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
700 1 _ |a Mandelkow, Eva Maria
|0 P:(DE-2719)2541658
|b 1
|e Last author
773 1 8 |a 10.1016/j.conb.2015.09.004
|b : Elsevier BV, 2016-02-01
|p 52-58
|3 journal-article
|2 Crossref
|t Current Opinion in Neurobiology
|v 36
|y 2016
|x 0959-4388
773 _ _ |a 10.1016/j.conb.2015.09.004
|g Vol. 36, p. 52 - 58
|0 PERI:(DE-600)2013035-1
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|p 52-58
|t Current opinion in neurobiology
|v 36
|y 2016
|x 0959-4388
909 C O |p VDB
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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