The DOI matches its Crossref record; 181 of the 181 references it cites were found in a registry or an index.
PPARs in the brain
Abstract
The biology of peroxisome proliferator activated receptors (PPARs) in physiological and pathophysiological processes has been primarily studied in peripherial organs and tissues. Recently it became clear that PPARs play an important role for the pathogenesis of various disorders of the CNS. The finding that activation of PPARs, and in particular, the PPARgamma isoform, suppresses inflammation in peripherial macrophages and in models of human autoimmune disease, instigated the experimental evaluation of these salutary actions for several CNS disorders that have an inflammatory component. Activation of all PPAR isoforms, but especially of PPARgamma, has been found to be protective in murine in vitro and in vivo models of Multiple Sclerosis. The verification of these findings in human cells prompted the initiation of clinical studies evaluating PPARgamma activation in Multiple Sclerosis patients. Likewise, Alzheimer's disease has a prominent inflammatory component that arises in response to neurodegeneration and to extracellular deposition of beta-amyloid peptides. The fact that non steroidal anti-inflammatory drugs (NSAIDs) delay the onset and reduce the risk to develop Alzheimer's disease, while they also bind to and activate PPARgamma, led to the hypothesis that one dimension of NSAID protection in AD may be mediated by PPARgamma. Several lines of evidence from in vitro and in vivo studies have supported this hypothesis, using Alzheimer disease related transgenic cellular and…
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“In the brain, PPAR␥ agonists reduce A-and cytokinemediated neuroinflammation and neurotoxicity in vitro (Heneka et al., 1999;Combs et al., 2000) and in vivo (for review, see Heneka and Landreth, 2007).”
From PPARγ/RXRα-Induced and CD36-Mediated Microglial Amyloid-β Phagocytosis Results in Cognitive Improvement in Amyloid Precursor Protein/Presenilin 1 Mice (2012) · cites this paper as Heneka and Landreth, 2007
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Metadata
- Authors
- HENEKA, M., & LANDRETH, G.
- Affiliations
- University of Münster (DE)
- Case Western Reserve University (US)
- Corresponding author
- HENEKA, M
- ORCID
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
- Publisher
- Elsevier BV
- Published
- 2007-08
- Volume
- 1771
- Issue
- 8
- Pages
- 1031-1045
- ISSN
- 1388-1981 (ISSN-L)
- OpenAlex
- W2054685711
- Cited by
- 317
- References
- 181
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 16 · 2023: 11 · 2022: 12 · 2021: 12 · 2020: 10 · 2019: 20 · 2018: 13 · 2017: 20 · 2016: 17 · 2015: 16 · 2014: 21 · 2013: 18 · 2012: 21
- FWCI
- 9.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- peroxisome proliferator-activated receptors, PPARγ, brain, neuroinflammation, multiple sclerosis, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, neurodegeneration, amyloid-beta, nonsteroidal anti-inflammatory drugs, PPAR agonists, neuroprotection, central nervous system development
- MeSH terms
- Animals, Brain, Brain Neoplasms, Central Nervous System Diseases, Brain Ischemia, Encephalomyelitis, Autoimmune, Experimental, Humans, Neurodegenerative Diseases, Peroxisome Proliferator-Activated Receptors
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