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- W2054685711 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 PPARγ 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 PPARγ, 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 PPARγ 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 β-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 PPARγ, led to the hypothesis that one dimension of NSAID protection in AD may be mediated by PPARγ. Several lines of evidence from in vitro and in vivo studies have supported this hypothesis, using Alzheimer disease related transgenic cellular and animal models. The ability of PPAR agonists to elicit anti-amyloidogenic, anti-inflammatory and insulin sensitizing effects may account for the observed effects. A number of clinical trials employing PPAR agonists have yielded promising results and further trials are in preparation, which aim to delineate the exact mechanism of interaction. Animal models of other neurodegenerative diseases such as Parkinson’s and Amyotrophic lateral sclerosis, both associated with a considerable degree of CNS inflammation, have been studied with a positive outcome. Yet it is not clear whether reduction of inflammation or additional mechanisms account for the observed neuroprotection. Less is known about the physiological role of PPARs for brain development, maintenance and function. Lesions from transgenic mouse models, however, provide evidence that PPARs may play pivotal roles for CNS development and function." @default.
- W2054685711 created "2016-06-24" @default.
- W2054685711 creator A5073496526 @default.
- W2054685711 creator A5078440867 @default.
- W2054685711 date "2007-08-01" @default.
- W2054685711 modified "2023-10-18" @default.
- W2054685711 title "PPARs in the brain" @default.
- W2054685711 cites W1491886022 @default.
- W2054685711 cites W1494611500 @default.
- W2054685711 cites W150222691 @default.
- W2054685711 cites W1530199299 @default.
- W2054685711 cites W1536266814 @default.
- W2054685711 cites W1539079080 @default.
- W2054685711 cites W1545110321 @default.
- W2054685711 cites W1557296944 @default.
- W2054685711 cites W1558213119 @default.
- W2054685711 cites W1574784740 @default.
- W2054685711 cites W1584270516 @default.
- W2054685711 cites W1585801143 @default.
- W2054685711 cites W1595492943 @default.
- W2054685711 cites W1629697287 @default.
- W2054685711 cites W1633340712 @default.
- W2054685711 cites W1639924204 @default.
- W2054685711 cites W164830943 @default.
- W2054685711 cites W1656162023 @default.
- W2054685711 cites W1659730200 @default.
- W2054685711 cites W1677573439 @default.
- W2054685711 cites W1678111194 @default.
- W2054685711 cites W1896225205 @default.
- W2054685711 cites W1896807099 @default.
- W2054685711 cites W1922073704 @default.
- W2054685711 cites W1925514517 @default.
- W2054685711 cites W1951826532 @default.
- W2054685711 cites W1964288033 @default.
- W2054685711 cites W1964671322 @default.
- W2054685711 cites W1966170928 @default.
- W2054685711 cites W1967564647 @default.
- W2054685711 cites W1967640260 @default.
- W2054685711 cites W1968703258 @default.
- W2054685711 cites W1970974990 @default.
- W2054685711 cites W1971153516 @default.
- W2054685711 cites W1971819432 @default.
- W2054685711 cites W1972248992 @default.
- W2054685711 cites W1973491513 @default.
- W2054685711 cites W1973868055 @default.
- W2054685711 cites W1975037850 @default.
- W2054685711 cites W1978881031 @default.
- W2054685711 cites W1978922638 @default.
- W2054685711 cites W1982971009 @default.
- W2054685711 cites W1985683101 @default.
- W2054685711 cites W1986933738 @default.
- W2054685711 cites W1987840903 @default.
- W2054685711 cites W1989584113 @default.
- W2054685711 cites W1995322895 @default.
- W2054685711 cites W1995574334 @default.
- W2054685711 cites W1996267589 @default.
- W2054685711 cites W1996892700 @default.
- W2054685711 cites W1997146656 @default.
- W2054685711 cites W1998630554 @default.
- W2054685711 cites W1998933601 @default.
- W2054685711 cites W1999890389 @default.
- W2054685711 cites W2001320540 @default.
- W2054685711 cites W2003115027 @default.
- W2054685711 cites W2005481412 @default.
- W2054685711 cites W2007015338 @default.
- W2054685711 cites W2008329724 @default.
- W2054685711 cites W2010233543 @default.
- W2054685711 cites W2011154010 @default.
- W2054685711 cites W2012662246 @default.
- W2054685711 cites W2014202196 @default.
- W2054685711 cites W2014941190 @default.
- W2054685711 cites W2015332596 @default.
- W2054685711 cites W2015402128 @default.
- W2054685711 cites W2018661263 @default.
- W2054685711 cites W2019026639 @default.
- W2054685711 cites W2019685247 @default.
- W2054685711 cites W2019970339 @default.
- W2054685711 cites W2022048961 @default.
- W2054685711 cites W2022378197 @default.
- W2054685711 cites W2023396428 @default.
- W2054685711 cites W2029177106 @default.
- W2054685711 cites W2029181833 @default.
- W2054685711 cites W2030305474 @default.
- W2054685711 cites W2031650186 @default.
- W2054685711 cites W2031919883 @default.
- W2054685711 cites W2034066397 @default.
- W2054685711 cites W2037076199 @default.
- W2054685711 cites W2037507488 @default.
- W2054685711 cites W2037971926 @default.
- W2054685711 cites W2039208165 @default.
- W2054685711 cites W2042584101 @default.
- W2054685711 cites W2042828511 @default.
- W2054685711 cites W2043841065 @default.
- W2054685711 cites W2045174329 @default.
- W2054685711 cites W2046833545 @default.
- W2054685711 cites W2047982128 @default.
- W2054685711 cites W2049761557 @default.
- W2054685711 cites W2053223105 @default.