001     138753
005     20240321220507.0
024 7 _ |a 10.3233/JAD-151135
|2 doi
024 7 _ |a pmid:27372638
|2 pmid
024 7 _ |a 1387-2877
|2 ISSN
024 7 _ |a 1875-8908
|2 ISSN
024 7 _ |a altmetric:9543235
|2 altmetric
037 _ _ |a DZNE-2020-05075
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Biella, Gloria
|b 0
245 _ _ |a Sirtuin 2 Inhibition Improves Cognitive Performance and Acts on Amyloid-β Protein Precursor Processing in Two Alzheimer's Disease Mouse Models.
260 _ _ |a Amsterdam
|c 2016
|b IOS Press
264 _ 1 |3 print
|2 Crossref
|b IOS Press
|c 2016-08-03
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1710940731_2065
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a The neuropathological hallmarks of Alzheimer's disease (AD) are extracellular plaques built up by the accumulation of the amyloid-β protein precursor (AβPP)-derived peptide β (Aβ), and intracellular tangles of hyperphosphorylated tau protein. Sirtuin 2 (SIRT2) is a member of the sirtuin family, featuring conserved enzymes with deacetylase activity and involved in several cell molecular pathways. We investigated the importance of SIRT2 inhibition in AD. We inhibited SIRT2 by small molecules (AGK-2, AK-7) and examined AβPP metabolism in H4-SW neuroglioma cells overexpressing AβPP and two AD transgenic mouse models (3xTg-AD and APP23). The in vitro studies suggested that the inhibition of SIRT2 reduced Aβ production; in vivo data showed an improvement of cognitive performance in the novel object recognition test, and an effect on AβPP proteolytic processing leading to a reduction of soluble β-AβPP and an increase of soluble α-AβPP protein. In 3xTg-AD mice, we noticed that total tau protein level rose. Overall, our pre-clinical data support a role for SIRT2 inhibition in the improvement of cognitive performance and the modulation of molecular mechanisms relevant for AD, thus deserving attention as possible therapeutic strategy.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a 3-(1-azepanylsulfonyl)-N-(3-bromphenyl)benzamide
|2 NLM Chemicals
650 _ 7 |a AGK2 compound
|2 NLM Chemicals
650 _ 7 |a Aif1 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Protein Precursor
|2 NLM Chemicals
650 _ 7 |a Benzamides
|2 NLM Chemicals
650 _ 7 |a Calcium-Binding Proteins
|2 NLM Chemicals
650 _ 7 |a Enzyme Inhibitors
|2 NLM Chemicals
650 _ 7 |a Furans
|2 NLM Chemicals
650 _ 7 |a Glial Fibrillary Acidic Protein
|2 NLM Chemicals
650 _ 7 |a Microfilament Proteins
|2 NLM Chemicals
650 _ 7 |a Peptide Fragments
|2 NLM Chemicals
650 _ 7 |a Quinolines
|2 NLM Chemicals
650 _ 7 |a Sulfonamides
|2 NLM Chemicals
650 _ 7 |a amyloid beta-protein (1-40)
|2 NLM Chemicals
650 _ 7 |a amyloid beta-protein (1-42)
|2 NLM Chemicals
650 _ 7 |a Sirtuin 2
|0 EC 3.5.1.-
|2 NLM Chemicals
650 _ 2 |a Alzheimer Disease: complications
|2 MeSH
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Benzamides: pharmacology
|2 MeSH
650 _ 2 |a Benzamides: therapeutic use
|2 MeSH
650 _ 2 |a Brain: drug effects
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Calcium-Binding Proteins: metabolism
|2 MeSH
650 _ 2 |a Cell Line, Tumor
|2 MeSH
650 _ 2 |a Cognition Disorders: drug therapy
|2 MeSH
650 _ 2 |a Cognition Disorders: etiology
|2 MeSH
650 _ 2 |a Cognition Disorders: metabolism
|2 MeSH
650 _ 2 |a Cognition Disorders: pathology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Enzyme Inhibitors: pharmacology
|2 MeSH
650 _ 2 |a Enzyme Inhibitors: therapeutic use
|2 MeSH
650 _ 2 |a Furans: pharmacology
|2 MeSH
650 _ 2 |a Furans: therapeutic use
|2 MeSH
650 _ 2 |a Gene Expression Regulation: drug effects
|2 MeSH
650 _ 2 |a Gene Expression Regulation: genetics
|2 MeSH
650 _ 2 |a Glial Fibrillary Acidic Protein: metabolism
|2 MeSH
650 _ 2 |a Glioma: pathology
|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 Microfilament Proteins: metabolism
|2 MeSH
650 _ 2 |a Peptide Fragments: metabolism
|2 MeSH
650 _ 2 |a Phosphorylation: drug effects
|2 MeSH
650 _ 2 |a Quinolines: pharmacology
|2 MeSH
650 _ 2 |a Quinolines: therapeutic use
|2 MeSH
650 _ 2 |a Sirtuin 2: metabolism
|2 MeSH
650 _ 2 |a Sulfonamides: pharmacology
|2 MeSH
650 _ 2 |a Sulfonamides: therapeutic use
|2 MeSH
700 1 _ |a Fusco, Federica
|b 1
700 1 _ |a Nardo, Emanuele
|b 2
700 1 _ |a Bernocchi, Ottavia
|b 3
700 1 _ |a Colombo, Alessio
|0 P:(DE-2719)2340744
|b 4
|u dzne
700 1 _ |a Lichtenthaler, Stefan F
|0 P:(DE-2719)2181459
|b 5
|u dzne
700 1 _ |a Forloni, Gianluigi
|b 6
700 1 _ |a Albani, Diego
|0 P:(DE-HGF)0
|b 7
|e Corresponding author
773 1 8 |a 10.3233/jad-151135
|b : IOS Press, 2016-08-03
|n 3
|p 1193-1207
|3 journal-article
|2 Crossref
|t Journal of Alzheimer's Disease
|v 53
|y 2016
|x 1387-2877
773 _ _ |a 10.3233/JAD-151135
|g Vol. 53, no. 3, p. 1193 - 1207
|0 PERI:(DE-600)2070772-1
|n 3
|q 53:3<1193 - 1207
|p 1193-1207
|t Journal of Alzheimer's disease
|v 53
|y 2016
|x 1387-2877
856 4 _ |u https://pub.dzne.de/record/138753/files/DZNE-2020-05075_Restricted.pdf
856 4 _ |u https://pub.dzne.de/record/138753/files/DZNE-2020-05075_Restricted.pdf?subformat=pdfa
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909 C O |p VDB
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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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|0 G:(DE-HGF)POF3-342
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914 1 _ |y 2016
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21