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| Home > Publications Database > PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice. > print |
| Home > Publications Database > PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice. > print |
| 001 | 136710 | ||
| 005 | 20240321220125.0 | ||
| 024 | 7 | _ | |a 10.1523/JNEUROSCI.1569-12.2012 |2 doi |
| 024 | 7 | _ | |a pmid:23197723 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC6621845 |2 pmc |
| 024 | 7 | _ | |a 0270-6474 |2 ISSN |
| 024 | 7 | _ | |a 1529-2401 |2 ISSN |
| 024 | 7 | _ | |a altmetric:4243638 |2 altmetric |
| 037 | _ | _ | |a DZNE-2020-03032 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Yamanaka, Mitsugu |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice. |
| 260 | _ | _ | |a Washington, DC |c 2012 |b Soc.57413 |
| 264 | _ | 1 | |3 online |2 Crossref |b Society for Neuroscience |c 2012-11-28 |
| 264 | _ | 1 | |3 print |2 Crossref |b Society for Neuroscience |c 2012-11-28 |
| 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 1586874853_30145 |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 Alzheimer's disease (AD) is characterized by the extracellular deposition of amyloid-β (Aβ), neurofibrillary tangle formation, and a microglial-driven inflammatory response. Chronic inflammatory activation compromises microglial clearance functions. Because peroxisome proliferator-activated receptor γ (PPARγ) agonists suppress inflammatory gene expression, we tested whether activation of PPARγ would also result in improved microglial Aβ phagocytosis. The PPARγ agonist pioglitazone and a novel selective PPARα/γ modulator, DSP-8658, currently in clinical development for the treatment of type 2 diabetes, enhanced the microglial uptake of Aβ in a PPARγ-dependent manner. This PPARγ-stimulated increase of Aβ phagocytosis was mediated by the upregulation of scavenger receptor CD36 expression. In addition, combined treatment with agonists for the heterodimeric binding partners of PPARγ, the retinoid X receptors (RXRs), showed additive enhancement of the Aβ uptake that was mediated by RXRα activation. Evaluation of DSP-8658 in the amyloid precursor protein/presenilin 1 mouse model confirmed an increased microglial Aβ phagocytosis in vivo, which subsequently resulted in a reduction of cortical and hippocampal Aβ levels. Furthermore, DSP-8658-treated mice showed improved spatial memory performance. Therefore, stimulation of microglial clearance by simultaneous activation of the PPARγ/RXRα heterodimer may prove beneficial in prevention of AD. |
| 536 | _ | _ | |a 344 - Clinical and Health Care Research (POF3-344) |0 G:(DE-HGF)POF3-344 |c POF3-344 |f POF III |x 0 |
| 542 | _ | _ | |i 2013-05-28 |2 Crossref |u https://creativecommons.org/licenses/by-nc-sa/4.0/ |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a Amyloid beta-Protein Precursor |2 NLM Chemicals |
| 650 | _ | 7 | |a Hypoglycemic Agents |2 NLM Chemicals |
| 650 | _ | 7 | |a PPAR gamma |2 NLM Chemicals |
| 650 | _ | 7 | |a Presenilin-1 |2 NLM Chemicals |
| 650 | _ | 7 | |a Thiazolidinediones |2 NLM Chemicals |
| 650 | _ | 7 | |a Pioglitazone |0 X4OV71U42S |2 NLM Chemicals |
| 650 | _ | 2 | |a Alzheimer Disease: drug therapy |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: metabolism |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: psychology |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 Behavior, Animal: drug effects |2 MeSH |
| 650 | _ | 2 | |a Behavior, Animal: physiology |2 MeSH |
| 650 | _ | 2 | |a Brain: drug effects |2 MeSH |
| 650 | _ | 2 | |a Brain: metabolism |2 MeSH |
| 650 | _ | 2 | |a Cognition: drug effects |2 MeSH |
| 650 | _ | 2 | |a Cognition: physiology |2 MeSH |
| 650 | _ | 2 | |a Disease Models, Animal |2 MeSH |
| 650 | _ | 2 | |a Hypoglycemic Agents: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Hypoglycemic Agents: therapeutic use |2 MeSH |
| 650 | _ | 2 | |a Maze Learning: drug effects |2 MeSH |
| 650 | _ | 2 | |a Maze Learning: physiology |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Microglia: drug effects |2 MeSH |
| 650 | _ | 2 | |a Microglia: metabolism |2 MeSH |
| 650 | _ | 2 | |a PPAR gamma: agonists |2 MeSH |
| 650 | _ | 2 | |a Phagocytosis: drug effects |2 MeSH |
| 650 | _ | 2 | |a Phagocytosis: physiology |2 MeSH |
| 650 | _ | 2 | |a Pioglitazone |2 MeSH |
| 650 | _ | 2 | |a Presenilin-1: genetics |2 MeSH |
| 650 | _ | 2 | |a Presenilin-1: metabolism |2 MeSH |
| 650 | _ | 2 | |a Thiazolidinediones: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Thiazolidinediones: therapeutic use |2 MeSH |
| 700 | 1 | _ | |a Ishikawa, Taizo |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Griep, Angelika |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Axt, Daisy |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Kummer, Markus P |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Heneka, Michael T |0 P:(DE-2719)2000008 |b 5 |e Last author |
| 773 | 1 | 8 | |a 10.1523/jneurosci.1569-12.2012 |b Society for Neuroscience |d 2012-11-28 |n 48 |p 17321-17331 |3 journal-article |2 Crossref |t The Journal of Neuroscience |v 32 |y 2012 |x 0270-6474 |
| 773 | _ | _ | |a 10.1523/JNEUROSCI.1569-12.2012 |g Vol. 32, no. 48, p. 17321 - 17331 |0 PERI:(DE-600)1475274-8 |n 48 |q 32:48<17321 - 17331 |p 17321-17331 |t The journal of neuroscience |v 32 |y 2012 |x 0270-6474 |
| 856 | 7 | _ | |2 Pubmed Central |u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6621845 |
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