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001     141416
005     20240321220944.0
024 7 _ |a 10.3233/JAD-2011-110320
|2 doi
024 7 _ |a pmid:21628793
|2 pmid
024 7 _ |a 1387-2877
|2 ISSN
024 7 _ |a 1875-8908
|2 ISSN
037 _ _ |a DZNE-2020-07738
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Ploia, Cristina
|b 0
245 _ _ |a JNK plays a key role in tau hyperphosphorylation in Alzheimer's disease models.
260 _ _ |a Amsterdam
|c 2011
|b IOS Press
264 _ 1 |3 print
|2 Crossref
|b IOS Press
|c 2011-09-09
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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|s 1710933999_2067
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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 Alzheimer's disease (AD) is a major clinical concern, and the search for new molecules to combat disease progression remains important. One of the major hallmarks in AD pathogenesis is the hyperphosphorylation of tau and subsequent formation of neurofibrillary tangles. Several kinases are involved in this process. Amongst them, c-Jun N-terminal kinases (JNKs) are activated in AD brains and are also associated with the development of amyloid plaques. This study was designed to investigate the contribution of JNK in tau hyperphosphorylation and whether it may represent a potential therapeutic target for the fight against AD. The specific inhibition of JNK by the cell permeable peptide D-JNKI-1 led to a reduction of p-tau at S202/T205 and S422, two established target sites of JNK, in rat neuronal cultures and in human fibroblasts cultures. Similarly, D-JNKI-1 reduced p-tau at S202/T205 in an in vivo model of AD (TgCRND8 mice). Our findings support the fundamental role of JNK in the regulation of tau hyperphosphorylation and subsequently in AD pathogenesis.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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|c POF3-342
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 7 |a JNK Mitogen-Activated Protein Kinases
|0 EC 2.7.11.24
|2 NLM Chemicals
650 _ 7 |a Mitogen-Activated Protein Kinases
|0 EC 2.7.11.24
|2 NLM Chemicals
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Aged, 80 and over
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Cells, Cultured
|2 MeSH
650 _ 2 |a Cerebral Cortex: drug effects
|2 MeSH
650 _ 2 |a Cerebral Cortex: metabolism
|2 MeSH
650 _ 2 |a Cerebral Cortex: pathology
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a JNK Mitogen-Activated Protein Kinases: metabolism
|2 MeSH
650 _ 2 |a JNK Mitogen-Activated Protein Kinases: pharmacology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Mitogen-Activated Protein Kinases: metabolism
|2 MeSH
650 _ 2 |a Neurofibrillary Tangles: drug effects
|2 MeSH
650 _ 2 |a Neurofibrillary Tangles: metabolism
|2 MeSH
650 _ 2 |a Neurofibrillary Tangles: pathology
|2 MeSH
650 _ 2 |a Neurons: drug effects
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Phosphorylation
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
700 1 _ |a Antoniou, Xanthi
|b 1
700 1 _ |a Sclip, Alessandra
|b 2
700 1 _ |a Grande, Valentina
|b 3
700 1 _ |a Cardinetti, Daniele
|b 4
700 1 _ |a Colombo, Alessio
|0 P:(DE-2719)2340744
|b 5
|u dzne
700 1 _ |a Canu, Nadia
|b 6
700 1 _ |a Benussi, Luisa
|b 7
700 1 _ |a Ghidoni, Roberta
|b 8
700 1 _ |a Forloni, Gianluigi
|b 9
700 1 _ |a Borsello, Tiziana
|0 P:(DE-HGF)0
|b 10
|e Corresponding author
773 1 8 |a 10.3233/jad-2011-110320
|b : IOS Press, 2011-09-09
|n 2
|p 315-329
|3 journal-article
|2 Crossref
|t Journal of Alzheimer's Disease
|v 26
|y 2011
|x 1875-8908
773 _ _ |a 10.3233/JAD-2011-110320
|g Vol. 26, no. 2, p. 315 - 329
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|n 2
|q 26:2<315 - 329
|p 315-329
|t Journal of Alzheimer's disease
|v 26
|y 2011
|x 1875-8908
856 4 _ |u https://pub.dzne.de/record/141416/files/DZNE-2020-07738_Restricted.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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