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000138753 0247_ $$2doi$$a10.3233/JAD-151135
000138753 0247_ $$2pmid$$apmid:27372638
000138753 0247_ $$2ISSN$$a1387-2877
000138753 0247_ $$2ISSN$$a1875-8908
000138753 0247_ $$2altmetric$$aaltmetric:9543235
000138753 037__ $$aDZNE-2020-05075
000138753 041__ $$aEnglish
000138753 082__ $$a610
000138753 1001_ $$aBiella, Gloria$$b0
000138753 245__ $$aSirtuin 2 Inhibition Improves Cognitive Performance and Acts on Amyloid-β Protein Precursor Processing in Two Alzheimer's Disease Mouse Models.
000138753 260__ $$aAmsterdam$$bIOS Press$$c2016
000138753 264_1 $$2Crossref$$3print$$bIOS Press$$c2016-08-03
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000138753 520__ $$aThe 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.
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000138753 650_7 $$2NLM Chemicals$$a3-(1-azepanylsulfonyl)-N-(3-bromphenyl)benzamide
000138753 650_7 $$2NLM Chemicals$$aAGK2 compound
000138753 650_7 $$2NLM Chemicals$$aAif1 protein, mouse
000138753 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000138753 650_7 $$2NLM Chemicals$$aAmyloid beta-Protein Precursor
000138753 650_7 $$2NLM Chemicals$$aBenzamides
000138753 650_7 $$2NLM Chemicals$$aCalcium-Binding Proteins
000138753 650_7 $$2NLM Chemicals$$aEnzyme Inhibitors
000138753 650_7 $$2NLM Chemicals$$aFurans
000138753 650_7 $$2NLM Chemicals$$aGlial Fibrillary Acidic Protein
000138753 650_7 $$2NLM Chemicals$$aMicrofilament Proteins
000138753 650_7 $$2NLM Chemicals$$aPeptide Fragments
000138753 650_7 $$2NLM Chemicals$$aQuinolines
000138753 650_7 $$2NLM Chemicals$$aSulfonamides
000138753 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-40)
000138753 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-42)
000138753 650_7 $$0EC 3.5.1.-$$2NLM Chemicals$$aSirtuin 2
000138753 650_2 $$2MeSH$$aAlzheimer Disease: complications
000138753 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000138753 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000138753 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000138753 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: genetics
000138753 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: metabolism
000138753 650_2 $$2MeSH$$aAnimals
000138753 650_2 $$2MeSH$$aBenzamides: pharmacology
000138753 650_2 $$2MeSH$$aBenzamides: therapeutic use
000138753 650_2 $$2MeSH$$aBrain: drug effects
000138753 650_2 $$2MeSH$$aBrain: metabolism
000138753 650_2 $$2MeSH$$aCalcium-Binding Proteins: metabolism
000138753 650_2 $$2MeSH$$aCell Line, Tumor
000138753 650_2 $$2MeSH$$aCognition Disorders: drug therapy
000138753 650_2 $$2MeSH$$aCognition Disorders: etiology
000138753 650_2 $$2MeSH$$aCognition Disorders: metabolism
000138753 650_2 $$2MeSH$$aCognition Disorders: pathology
000138753 650_2 $$2MeSH$$aDisease Models, Animal
000138753 650_2 $$2MeSH$$aEnzyme Inhibitors: pharmacology
000138753 650_2 $$2MeSH$$aEnzyme Inhibitors: therapeutic use
000138753 650_2 $$2MeSH$$aFurans: pharmacology
000138753 650_2 $$2MeSH$$aFurans: therapeutic use
000138753 650_2 $$2MeSH$$aGene Expression Regulation: drug effects
000138753 650_2 $$2MeSH$$aGene Expression Regulation: genetics
000138753 650_2 $$2MeSH$$aGlial Fibrillary Acidic Protein: metabolism
000138753 650_2 $$2MeSH$$aGlioma: pathology
000138753 650_2 $$2MeSH$$aMice
000138753 650_2 $$2MeSH$$aMice, Inbred C57BL
000138753 650_2 $$2MeSH$$aMice, Transgenic
000138753 650_2 $$2MeSH$$aMicrofilament Proteins: metabolism
000138753 650_2 $$2MeSH$$aPeptide Fragments: metabolism
000138753 650_2 $$2MeSH$$aPhosphorylation: drug effects
000138753 650_2 $$2MeSH$$aQuinolines: pharmacology
000138753 650_2 $$2MeSH$$aQuinolines: therapeutic use
000138753 650_2 $$2MeSH$$aSirtuin 2: metabolism
000138753 650_2 $$2MeSH$$aSulfonamides: pharmacology
000138753 650_2 $$2MeSH$$aSulfonamides: therapeutic use
000138753 7001_ $$aFusco, Federica$$b1
000138753 7001_ $$aNardo, Emanuele$$b2
000138753 7001_ $$aBernocchi, Ottavia$$b3
000138753 7001_ $$0P:(DE-2719)2340744$$aColombo, Alessio$$b4$$udzne
000138753 7001_ $$0P:(DE-2719)2181459$$aLichtenthaler, Stefan F$$b5$$udzne
000138753 7001_ $$aForloni, Gianluigi$$b6
000138753 7001_ $$0P:(DE-HGF)0$$aAlbani, Diego$$b7$$eCorresponding author
000138753 77318 $$2Crossref$$3journal-article$$a10.3233/jad-151135$$b : IOS Press, 2016-08-03$$n3$$p1193-1207$$tJournal of Alzheimer's Disease$$v53$$x1387-2877$$y2016
000138753 773__ $$0PERI:(DE-600)2070772-1$$a10.3233/JAD-151135$$gVol. 53, no. 3, p. 1193 - 1207$$n3$$p1193-1207$$q53:3<1193 - 1207$$tJournal of Alzheimer's disease$$v53$$x1387-2877$$y2016
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