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@ARTICLE{Katsouri:136269,
      author       = {Katsouri, Loukia and Parr, Callum and Bogdanovic, Nenad and
                      Willem, Michael and Sastre, Magdalena},
      title        = {{PPAR}γ co-activator-1α ({PGC}-1α) reduces amyloid-β
                      generation through a {PPAR}γ-dependent mechanism.},
      journal      = {Journal of Alzheimer's disease},
      volume       = {25},
      number       = {1},
      issn         = {1875-8908},
      address      = {Amsterdam},
      publisher    = {IOS Press},
      reportid     = {DZNE-2020-02591},
      pages        = {151-162},
      year         = {2011},
      abstract     = {We 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.},
      keywords     = {Aged / Aged, 80 and over / Alzheimer Disease: metabolism /
                      Alzheimer Disease: pathology / Amyloid beta-Peptides:
                      antagonists $\&$ inhibitors / Amyloid beta-Peptides:
                      biosynthesis / Animals / Cell Line, Tumor / Down-Regulation:
                      physiology / Female / Heat-Shock Proteins: antagonists $\&$
                      inhibitors / Heat-Shock Proteins: physiology / Humans / Male
                      / Mice / Middle Aged / PPAR gamma: physiology / Peroxisome
                      Proliferator-Activated Receptor Gamma Coactivator 1-alpha /
                      Transcription Factors: antagonists $\&$ inhibitors /
                      Transcription Factors: physiology / Amyloid beta-Peptides
                      (NLM Chemicals) / Heat-Shock Proteins (NLM Chemicals) / PPAR
                      gamma (NLM Chemicals) / PPARGC1A protein, human (NLM
                      Chemicals) / Peroxisome Proliferator-Activated Receptor
                      Gamma Coactivator 1-alpha (NLM Chemicals) / Transcription
                      Factors (NLM Chemicals)},
      cin          = {Ext LMU},
      ddc          = {610},
      cid          = {I:(DE-2719)5000048},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21358044},
      doi          = {10.3233/JAD-2011-101356},
      url          = {https://pub.dzne.de/record/136269},
}