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000136269 0247_ $$2doi$$a10.3233/JAD-2011-101356
000136269 0247_ $$2pmid$$apmid:21358044
000136269 0247_ $$2ISSN$$a1387-2877
000136269 0247_ $$2ISSN$$a1875-8908
000136269 0247_ $$2altmetric$$aaltmetric:49675411
000136269 037__ $$aDZNE-2020-02591
000136269 041__ $$aEnglish
000136269 082__ $$a610
000136269 1001_ $$aKatsouri, Loukia$$b0
000136269 245__ $$aPPARγ co-activator-1α (PGC-1α) reduces amyloid-β generation through a PPARγ-dependent mechanism.
000136269 260__ $$aAmsterdam$$bIOS Press$$c2011
000136269 264_1 $$2Crossref$$3print$$bIOS Press$$c2011-06-14
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000136269 520__ $$aWe have previously reported that the nuclear receptor peroxisome proliferator activated receptor-γ (PPARγ) regulates the transcription of β-secretase (BACE1), a key enzyme involved in amyloid-β (Aβ) generation. Here, we aimed to investigate the role of PPARγ coactivator-1α (PGC-1α), which controls major metabolic functions through the co-activation of PPARγ and other transcription factors. Western blotting experiments with nuclear extracts from brain cortex of AD cases and controls showed a reduction in the levels of PGC-1α in AD patients. PGC-1α overexpression in N2a neuroblastoma cells induced a decrease in the levels of secreted Aβ and an increase in the levels of non-amyloidogenic soluble AβPPα. The decrease in Aβ after exogenous expression of PGC-1α was a consequence of reduced BACE1 expression and transcription, together with a decrease in BACE1 promoter activity. In addition, we detected a significant reduction in β-secretase activity by measuring the levels of β-carboxy terminus fragment (β-CTFs) and by using a commercial assay for β-secretase. In contrast, down-regulation of PGC-1α levels by transfection with PGC-1α siRNA increased BACE1 expression. These effects appeared to be dependent on PPARγ, because PGC-1α did not affect Aβ and BACE1 levels in N2a cells transfected with PPARγ siRNA or in PPARγ knockout fibroblasts. In conclusion, since PGC-1α appears to decrease Aβ generation, therapeutic modulation of PGC-1α could have real potential as a treatment for AD.
000136269 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
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000136269 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000136269 650_7 $$2NLM Chemicals$$aHeat-Shock Proteins
000136269 650_7 $$2NLM Chemicals$$aPPAR gamma
000136269 650_7 $$2NLM Chemicals$$aPPARGC1A protein, human
000136269 650_7 $$2NLM Chemicals$$aPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
000136269 650_7 $$2NLM Chemicals$$aTranscription Factors
000136269 650_2 $$2MeSH$$aAged
000136269 650_2 $$2MeSH$$aAged, 80 and over
000136269 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000136269 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000136269 650_2 $$2MeSH$$aAmyloid beta-Peptides: antagonists & inhibitors
000136269 650_2 $$2MeSH$$aAmyloid beta-Peptides: biosynthesis
000136269 650_2 $$2MeSH$$aAnimals
000136269 650_2 $$2MeSH$$aCell Line, Tumor
000136269 650_2 $$2MeSH$$aDown-Regulation: physiology
000136269 650_2 $$2MeSH$$aFemale
000136269 650_2 $$2MeSH$$aHeat-Shock Proteins: antagonists & inhibitors
000136269 650_2 $$2MeSH$$aHeat-Shock Proteins: physiology
000136269 650_2 $$2MeSH$$aHumans
000136269 650_2 $$2MeSH$$aMale
000136269 650_2 $$2MeSH$$aMice
000136269 650_2 $$2MeSH$$aMiddle Aged
000136269 650_2 $$2MeSH$$aPPAR gamma: physiology
000136269 650_2 $$2MeSH$$aPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
000136269 650_2 $$2MeSH$$aTranscription Factors: antagonists & inhibitors
000136269 650_2 $$2MeSH$$aTranscription Factors: physiology
000136269 7001_ $$aParr, Callum$$b1
000136269 7001_ $$aBogdanovic, Nenad$$b2
000136269 7001_ $$0P:(DE-2719)9000433$$aWillem, Michael$$b3$$udzne
000136269 7001_ $$0P:(DE-HGF)0$$aSastre, Magdalena$$b4$$eCorresponding author
000136269 77318 $$2Crossref$$3journal-article$$a10.3233/jad-2011-101356$$b : IOS Press, 2011-06-14$$n1$$p151-162$$tJournal of Alzheimer's Disease$$v25$$x1875-8908$$y2011
000136269 773__ $$0PERI:(DE-600)2070772-1$$a10.3233/JAD-2011-101356$$gVol. 25, no. 1, p. 151 - 162$$n1$$p151-162$$q25:1<151 - 162$$tJournal of Alzheimer's disease$$v25$$x1875-8908$$y2011
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000136269 9141_ $$y2011
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