HUGO ID Detailed Result 9236


HUGO ID 9236
Symbol PPARG
Name peroxisome proliferator-activated receptor gamma
#Occurrence 304
#Paper 10

 


PMID Match String Actual String Score Flanking text Edited by Edit
15649489PPARPPAR-G2.2the therapeutic effect of pioglitazone a peroxisome proliferator-activated receptor-gamma (PPAR-_amp_#x3b3;) PPAR-_amp_#x3b3 agonist in the G93A SOD1 transgenic mouse model of ALS 
15649489PPARPPAR-G2.2Previous studies showed that PPAR-_amp_#x3b3 agonists protect cerebellar granule cells from cytokine-induced apoptotic cell death 
15649489PPARPPAR-G2.2We therefore examined whether an agonist of PPAR-_amp_#x3b3 an anti-inflammatory protein could delay or slow the disease process 
15649489PPARPPAR-G2.2It was suggested that these effects were due to PPAR-_amp_#x3b3 activation an increase in inhibitory protein-_amp_#x3ba -_amp_#x3b2 expression and inhibition 
15649489PPARPPAR-G2.2PPAR-_amp_#x3b3 was originally characterized as a regulator of adipocyte differentiation and 
15649489PPARPPAR-G2.2PPAR-_amp_#x3b3 was also shown to have a possible role in cell 
15649489PPARPPAR-G2.2These authors showed anti-inflammatory effect of PPAR-_amp_#x3b3 15d-PGJ 2 in a rat model of carrageenin-induced pleural inflammation 
15649489PPARPPAR-G2.2Our data suggest that the neuroprotective effect of PPAR-_amp_#x3b3 may stem from its role in inflammation however other roles 
15649489PPARPPAR-G2.2stem from its role in inflammation however other roles of PPAR-_amp_#x3b3 may have contributed 
15649489PPARPPAR-G2.2of pioglitazone is not known obviously those cells that express PPAR-_amp_#x3b3 _amp_#xa0 would be targeted 
16753239PPARPPAR-G1.9commonly prescribed for the treatment of type II diabetes are PPAR-_amp_#x3b3 ligands 
16753239PPARPPAR-G1.9Naturally occurring PPAR-_amp_#x3b3 ligands include eicosanoids polyunsaturated fatty acids and the cyclopentenone prostaglandin 
16753239PPARPPAR-G1.9NSAID including indomethacin which are used to treat inflammation are PPAR-_amp_#x3b3 ligands 
16753239PPARPPAR-G1.9Critical early studies in this field demonstrated that PPAR-_amp_#x3b3 agonists are capable of suppressing immune activation of monocyte/macrophages monocyte 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 agonists are believed to suppress immune responses principally through transrepression 
16753239PPARPPAR-G1.9The PPAR-_amp_#x3b3 agonist 15d-PGJ 2 can regulate gene expression through receptor-independent mechanisms 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 
16753239PPARPPAR-G1.9The PPAR-_amp_#x3b3 agonist 15d-PGJ 2 was demonstrated to inhibit NO IL-1_amp_#x3b2 and 
16753239PPARPPAR-G1.9The PPAR-_amp_#x3b3 agonist troglitazone did not suppress the expression of these pro-inflammatory 
16753239PPARPPAR-G1.9by BV-2 cells suggesting that 15d-PGJ 2 may act through PPAR-_amp_#x3b3 -independent mechanisms ( Petrova et al. 1999 
16753239PPARPPAR-G1.9However since the PPAR-_amp_#x3b3 agonist ciglitazone suppressed the production of these pro-inflammatory molecules in 
16753239PPARPPAR-G1.9similar manner 15d-PGJ 2 was interpreted to act through a PPAR-_amp_#x3b3 dependent mechanism 
16753239PPARPPAR-G1.9In these studies HCT1026 activated the PPAR-_amp_#x3b3 receptor in microglia and the PPAR-_amp_#x3b3 antagonist GW9662 blocked receptor 
16753239PPARPPAR-G1.9studies HCT1026 activated the PPAR-_amp_#x3b3 receptor in microglia and the PPAR-_amp_#x3b3 antagonist GW9662 blocked receptor activation ( Bernardo et al. 2005 
16753239PPARPPAR-G1.9The basis for the discrepancy between these studies concerning whether PPAR-_amp_#x3b3 agonists influence microglial cell function through PPAR-_amp_#x3b3 -dependent or -independent 
16753239PPARPPAR-G1.9studies concerning whether PPAR-_amp_#x3b3 agonists influence microglial cell function through PPAR-_amp_#x3b3 -dependent or -independent mechanisms may be explained by the fact 
16753239PPARPPAR-G1.9conducted with BV-2 microglial cells which express little or no PPAR-_amp_#x3b3 
16753239PPARPPAR-G1.9molecules in spite of the fact that this agonist binds PPAR-_amp_#x3b3 with lower affinity than thiazolidinediones 
16753239PPARPPAR-G1.9RA may inhibit cell activation through the formation of PPAR-_amp_#x3b3;/RXR PPAR-_amp_#x3b3 RXR heterodimers 
16753239PPARPPAR-G1.9The expression of PPAR-_amp_#x3b3 increases in microglia and astrocytes during EAE supporting a role 
16753239PPARPPAR-G1.9is a cyclopentenone prostaglandin but is not believed to bind PPAR-_amp_#x3b3 is a potent inhibitor of the activation of primary mouse 
16753239PPARPPAR-G1.9suggest that 15d-PGJ 2 likely inhibits glial cell activation by PPAR-_amp_#x3b3 -dependent as well as PPAR-_amp_#x3b3 -independent mechanisms 
16753239PPARPPAR-G1.9inhibits glial cell activation by PPAR-_amp_#x3b3 -dependent as well as PPAR-_amp_#x3b3 -independent mechanisms 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 agonists are capable of inhibiting inflammatory responses in glia through 
16753239PPARPPAR-G1.9(2004) 2004 demonstrated that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 inhibited LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 
16753239PPARPPAR-G1.9Over expression of wild-type and dominant-negative constructs of PPAR-_amp_#x3b3 or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and 
16753239PPARPPAR-G1.9expression of wild-type and dominant-negative constructs of PPAR-_amp_#x3b3 or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and iNOS expression in 
16753239PPARPPAR-G1.9(2003) 2003 demonstrated that the PPAR-_amp_#x3b3 agonists 15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 agonist suppression of glial activation can have profound effects on 
16753239PPARPPAR-G1.9These studies further demonstrated that a variety of PPAR-_amp_#x3b3 agonists including TZDs 15d-PGJ 2 and NSAIDS blocked _amp_#x3b2 -amyloid 
16753239PPARPPAR-G1.9For example these PPAR-_amp_#x3b3 agonists blocked TNF-_amp_#x3b1 and IL-6 expression by monocytes 
16753239PPARPPAR-G1.9Collectively this study demonstrated that PPAR-_amp_#x3b3 agonists suppress the production by monocyte/microglial monocyte microglial cells of 
16753239PPARPPAR-G1.9by studies utilizing rat cortical neuron-glial co-cultures that indicated that PPAR-_amp_#x3b3 agonists including TZDs and 15d-PGJ 2 suppressed LPS induction of 
16753239PPARPPAR-G1.9A PPAR-_amp_#x3b3 antagonist blocked TZD protection of cortical neurons in these studies 
16753239PPARPPAR-G1.9Interestingly PPARs including PPAR-_amp_#x3b3 can be expressed by neurons ( Cimini et al. 2005 
16753239PPARPPAR-G1.9are required to more definitively determine the mechanisms by which PPAR-_amp_#x3b3 agonists modulate inflammatory responses in the CNS 
16753239PPARPPAR-G1.9or receptor-independent mechanisms are complicated by the paucity of specific PPAR-_amp_#x3b3 agonists and the fact that PPAR-_amp_#x3b3 -deficient mice die soon 
16753239PPARPPAR-G1.9the paucity of specific PPAR-_amp_#x3b3 agonists and the fact that PPAR-_amp_#x3b3 -deficient mice die soon after birth 
16753239PPARPPAR-G1.9In addition PPAR-_amp_#x3b3 agonists have been demonstrated in some studies to function through 
16753239PPARPPAR-G1.9The development of highly selective PPAR-_amp_#x3b3 antagonists and conditional PPAR-_amp_#x3b3 deficient mouse strains will be essential 
16753239PPARPPAR-G1.9The development of highly selective PPAR-_amp_#x3b3 antagonists and conditional PPAR-_amp_#x3b3 deficient mouse strains will be essential in determining the mechanisms 
16753239PPARPPAR-G1.9strains will be essential in determining the mechanisms by which PPAR-_amp_#x3b3 agonists control CNS inflammation 
16753239PPARPPAR-G1.9This suggests that like PPAR-_amp_#x3b3 and PPAR-_amp_#x3b1 agonists PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists may suppress chronic 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 
16753239PPARPPAR-G1.9(2001) 2001 first demonstrated that the PPAR-_amp_#x3b3 agonist troglitazone inhibited the development of EAE 
16753239PPARPPAR-G1.9(2002) 2002 showed that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 inhibited T cell proliferation 
16753239PPARPPAR-G1.9Natarajan and Bright (2002) 2002 demonstrated that the PPAR-_amp_#x3b3 agonists 15d-PGJ 2 and ciglitazone decreased the severity of both 
16753239PPARPPAR-G1.9(2003) 2003 also demonstrated that PPAR-_amp_#x3b3 deficient heterozygous mice exhibit more severe EAE than wild-type mice 
16753239PPARPPAR-G1.9These studies cannot be performed in PPAR-_amp_#x3b3 homozygous knockout mice which die en utero suggesting that PPAR-_amp_#x3b3 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 homozygous knockout mice which die en utero suggesting that PPAR-_amp_#x3b3 plays a critical role in development which cannot be compensated 
16753239PPARPPAR-G1.9Future studies utilizing inducible promoters to knock out PPAR-_amp_#x3b3 in adult mice are needed to confirm the role of 
16753239PPARPPAR-G1.9(2005) 2005 demonstrated that PPAR-_amp_#x3b3 antagonists exacerbate EAE 
16753239PPARPPAR-G1.9Collectively these studies suggest that PPAR-_amp_#x3b3 plays an important role in modulating the development of EAE 
16753239PPARPPAR-G1.9Interestingly this suggests that PPAR-_amp_#x3b3 and RXR ligands could act cooperatively in the treatment of 
16753239PPARPPAR-G1.9of MS A small clinical study supports the idea that PPAR-_amp_#x3b3 agonists may be effective in the treatment of MS ( 
16753239PPARPPAR-G1.9clinical trials are needed to assess the therapeutic potential of PPAR-_amp_#x3b3 agonists for the treatment of MS 
16753239PPARPPAR-G1.9the development of EAE and MS We demonstrated that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 selectively inhibits microglial expression of CD40 but 
16753239PPARPPAR-G1.9This suggests that PPAR-_amp_#x3b3 agonists may modulate EAE in part by affecting microglia-T cell 
16753239PPARPPAR-G1.9The studies outlined above suggest that PPAR-_amp_#x3b3 agonists may inhibit EAE at least in part by blocking 
16753239PPARPPAR-G1.9an important role in initiating EAE and MS In fact PPAR-_amp_#x3b3 agonists likely modulate the development of these disorders by a 
16753239PPARPPAR-G1.9For example PPAR-_amp_#x3b3 agonists were demonstrated to improve clinical outcomes in animal models 
16753239PPARPPAR-G1.9(2000) 2000 demonstrated that Tg2576 mice fed the PPAR-_amp_#x3b3 agonist ibuprofen for 6 months beginning at an age of 
16753239PPARPPAR-G1.9The role of PPAR-_amp_#x3b3 agonists in modulating the development of AD was further supported 
16753239PPARPPAR-G1.9Collectively these studies suggest that PPAR-_amp_#x3b3 agonists may be effective in the treatment of AD 
16753239PPARPPAR-G1.9dramatically inhibited glial activation in these studies suggesting that this PPAR-_amp_#x3b3 agonist may protect tyrosine hydroxylase positive neurons by controlling glial 
16753239PPARPPAR-G1.9Recent reports demonstrate that the PPAR-_amp_#x3b3 agonist pioglitazone protected motor neurons improved motor performance and extended 
16753239PPARPPAR-G1.9The PPAR-_amp_#x3b3 agonists troglitazone and pioglitazone reduced infarct volume and improved neurological 
16753239PPARPPAR-G1.9infarct volume was reduced and neurological function was improved by PPAR-_amp_#x3b3 agonist treatment when measured 22 days after the ischemic event 
16753239PPARPPAR-G1.9This suggests that PPAR-_amp_#x3b3 agonists may be therapeutic in humans following stroke 
16753239PPARPPAR-G1.9This suggests that PPAR-_amp_#x3b3 agonists may modulate events that occur following reperfusion 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 agonists reduced CNS inflammation including macrophage/microglial macrophage microglial activation following 
16753239PPARPPAR-G1.9PPAR-_amp_#x3b3 agonists of the thiazolidinedione class are currently prescribed for the 
18312546PPARGPPARgamma1.2Effects of the PPARgamma activator pioglitazone on p38 MAP kinase and IkappaBalpha in the 
18312546PPARGPPARgamma1.2molecular pathological effects of the anti-inflammatory peroxisome proliferator-activated receptor-gamma (PPARgamma) PPARgamma agonist pioglitazone in ALS we verified changes in the population 
18312546PPARGPPARgamma1.2littermates (control control mice performed immunohistochemical and immunoblot analyses of PPARgamma active form of phosphorylated p38 mitogen-activated protein kinase (p-p38) p-p38 
18312546PPARGPPARgamma1.2Immunohistochemical analysis demonstrated that immunoreactivities for PPARgamma and p-p38 were mainly localized in neurons and that IkappaBalpha 
18312546PPARGPPARgamma-immunoreactive1.2that pioglitazone treatment resulted in no significant change in nuclear PPARgamma-immunoreactive density a significant decrease in cytosolic p-p38-immunoreactive density and a 
18312546PPARGPPARgamma-independent1.2against p38-mediated neuronal death and NF-kappaB-mediated glial inflammation via a PPARgamma-independent mechanism 
18464922PPARPPAR-G2.2is described that can be activated by peroxisome proliferator-activated receptor-_amp_#x003b3 PPAR-_amp_#x003b3 agonists and has the ability to block the neuropathological damage 
18464922PPARPPAR-G2.2Therefore PPAR-_amp_#x003b3 agonists are thought to be neuroprotective in ALS and HD 
18464922PPARPPAR-G2.2have tested the neuroprotective effect of pioglitazone (Actos), Actos a PPAR-_amp_#x003b3 agonist in G93A SOD1 transgenic mouse model of ALS and 
18464922PPARPPAR-G2.2These findings suggest that PPAR-_amp_#x003b3 may be an important regulator of neuroinflammation and possibly a 
18464922PPARPPAR-G2.2The involvement of PPAR-_amp_#x003b3 in HD is currently under investigation one study finds that 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 coactivator-1 _amp_#x003b1 (PGC-1 PGC-1 _amp_#x003b1 is a transcriptional coactivator that 
18464922PPARPPAR-G2.2that works together with combination of other transcription factors like PPAR-_amp_#x003b3 in the regulation of mitochondrial biogenesis 
18464922PPARPPAR-G2.2Therefore PPAR-_amp_#x003b3 is a possible target for ALS and HD as it 
18464922PPARPPAR-G2.2In this review the role of PPAR-_amp_#x003b3 in ALS and HD is discussed based on the current 
18464922PPARPPAR-G2.2that belong to the nuclear hormone receptor superfamily which includes PPAR-_amp_#x003b3 PPAR-_amp_#x003b1 and PPAR-_amp_#x003b2 / _amp_#x003b4 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 is the most studied receptor and has two isoforms produced 
18464922PPARPPAR-G2.2isoforms produced due to alternative splicing and alternate translation initiation PPAR-_amp_#x003b3 1 and PPAR-_amp_#x003b3 2 1 2 
18464922PPARPPAR-G2.2to alternative splicing and alternate translation initiation PPAR-_amp_#x003b3 1 and PPAR-_amp_#x003b3 2 1 2 
18464922PPARPPAR-G2.2and _amp_#x003b4 appear primarily to stimulate oxidative lipid metabolism while PPAR-_amp_#x003b3 is principally involved in the cellular assimilation of lipids via 
18464922PPARPPAR-G2.2Recently other functions for PPAR-_amp_#x003b3 are described such as neuroprotection in ischemia 15 and its 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 has been demonstrated to be involved in adipogenesis and differentiation 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 is shown to have a vital role in adipocyte differentiation 
18464922PPARPPAR-G2.2Recent studies demonstrate PPAR-_amp_#x003b3 agonists to prevent inflammation and neuronal death after focal cerebral 
18464922PPARPPAR-G2.2Thiazolidinediones (TZDs) TZDs are potent synthetic agonists of PPAR-_amp_#x003b3 shown to induce neuroprotection after cerebral ischemia by blocking inflammation 
18464922PPARPPAR-G2.2protective lipid-independent effects of TZDs are the anti-inflammatory capacities of PPAR-_amp_#x003b3 4 
18464922PPARPPAR-G2.2transducers and activators of transcription (STAT) STAT transcription factors by PPAR-_amp_#x003b3 31 
18464922PPARPPAR-G2.2It is possible that PPAR-_amp_#x003b3 is involved in the reciprocal inhibition of differential transcription systems 
18464922PPARPPAR-G2.2an alternative mechanism suggested that a functionally distinct pool of PPAR-_amp_#x003b3 is susceptible to ligand-dependent sumoylation (covalent covalent attachment of small 
18464922PPARPPAR-G2.2of neuronal cell death in ALS and a representation of PPAR-_amp_#x003b3 activation 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 AND AMYOTROPHIC LATERAL SCLEROSIS 
18464922PPARPPAR-G2.2PPARs in particular PPAR-_amp_#x003b3 may be a major signaling pathway involved in neuroinflammation in 
18464922PPARPPAR-G2.2The activation or inactivation of PPAR-_amp_#x003b3 could provide a viable and promising approach to understand the 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 has been identified as a key regulatory factor in the 
18464922PPARPPAR-G2.2Synthetic PPAR-_amp_#x003b3 agonists developed in the past 25 years that are used 
18464922PPARPPAR-G2.2suitable candidates and are indispensable to study the role of PPAR-_amp_#x003b3 in ALS which may potentially lead to beneficial effects in 
18464922PPARPPAR-G2.2Previous studies have shown the protective effect of PPAR-_amp_#x003b3 agonists in many experimental models such as in experimental autoimmune 
18464922PPARPPAR-G2.2Additionally PPAR-_amp_#x003b3 agonists are reported to be neuroprotective in tyrosine hydroxylase positive 
18464922PPARPPAR-G2.2In this study PPAR-_amp_#x003b3 agonist treatment improved survival muscle strength and weight loss in 
18464922PPARPPAR-G2.2Other studies using PPAR-_amp_#x003b3 agonists suggest that the mechanism of actions are also by 
18464922PPARPPAR-G2.2Recently Xu and Drew demonstrated that PPAR-_amp_#x003b3 agonists suppress cytokines like IL-12 family in EAE an experimental 
18464922PPARPPAR-G2.2These studies provide evidence that PPAR-_amp_#x003b3 agonist responses are originating from activated glial cells in central 
18464922PPARPPAR-G2.2showed reduction in gliosis which is another experimental evidence that PPAR-_amp_#x003b3 acts on glial cells in CNS 38 
18464922PPARPPAR-G2.2The action of PPAR-_amp_#x003b3 in neuronal cells needs to be studied 
18464922PPARPPAR-G2.2The preliminary reports on the neuroprotective role of PPAR-_amp_#x003b3 agonist in transgenic mouse model of ALS and other experimental 
18464922PPARPPAR-G2.2The mechanisms of how PPAR-_amp_#x003b3 agonists induce neuroprotection by blocking neuroinflammation is not fully understood 
18464922PPARPPAR-G2.2fully understood and further information on the molecular details of PPAR-_amp_#x003b3 in neuroinflammatory pathways will provide crucial insights on the role 
18464922PPARPPAR-G2.2neuroinflammatory pathways will provide crucial insights on the role of PPAR-_amp_#x003b3 in ALS and other neurodegenerative diseases 
18464922PPARPPAR-G2.2Since PGC-1 _amp_#x003b1 is a PPAR-_amp_#x003b3 coactivator it is possible that PPAR-_amp_#x003b3 agonists may be able 
18464922PPARPPAR-G2.2PGC-1 _amp_#x003b1 is a PPAR-_amp_#x003b3 coactivator it is possible that PPAR-_amp_#x003b3 agonists may be able to activate PGC-1 _amp_#x003b1 and also 
18464922PPARPPAR-G2.2Whether mutant SOD1 can impair PPAR-_amp_#x003b3 is yet to be determined 
18464922PPARPPAR-G2.2Future studies on PGC-1 _amp_#x003b1 and PPAR-_amp_#x003b3 in ALS patients and transgenic mice will shed some lights 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 AND HUNTINGTON'S DISEASE 
18464922PPARPPAR-G2.2Recent reports show that mutant huntingtin interferes with transcriptional PPAR-_amp_#x003b3 coactivator-1 _amp_#x003b1 (PGC-1 PGC-1 _amp_#x003b1 causing impairment on its function 
18464922PPARPPAR-G2.2and R.E Hughes that their yeast two-hybrid screen identified that PPAR-_amp_#x003b3 is a huntingtin interactor and the interaction was validated for 
18464922PPARPPAR-G2.2validated for its biological significance by demonstrating an effect of PPAR-_amp_#x003b3 dosage upon HD neurodegeneration in the fly eye 27 
18464922PPARPPAR-G2.2must be explored in order to understand the role of PPAR-_amp_#x003b3 and to identify new therapeutic targets for HD 
18464922PPARPPAR-G2.2Rosiglitazone (a a PPAR-_amp_#x003b3 agonist that induces sensitization to insulin was tested in R6/2 
18464922PPARPPAR-G2.22 mice it also provided data for the role of PPAR-_amp_#x003b3 in R6/2 R6 2 mice 
18464922PPARPPAR-G2.2Rosiglitazone was used as PPAR-_amp_#x003b3 agonist in R6/2 R6 2 mice which could be used 
18464922PPARPPAR-G2.2be used as the bases to test the role of PPAR-_amp_#x003b3 in HD glibenclamide and metformin were used to treat atypical 
18464922PPARPPAR-G2.2Metformin does not belong to any class of PPAR-_amp_#x003b3 agonists although it is an antidiabetic for type-2 diabetes and 
18464922PPARPPAR-G2.2shown to activate sirtuin 1 (SIRT1) SIRT1 and results in PPAR-_amp_#x003b3 -mediated transcriptional repression inhibition of adipogenesis enhanced lipolysis and the 
18464922PPARPPAR-G2.2Although PPAR-_amp_#x003b3 agonist treatments in R6/2 R6 2 failed it is premature 
18464922PPARPPAR-G2.2in other models of HD are required to examine other PPAR-_amp_#x003b3 agonists 
18464922PPARPPAR-G2.2Moreover the effect of PPAR-_amp_#x003b3 agonists on the expression and activation of PGC-1 _amp_#x003b1 in 
18464922PPARPPAR-G2.2oxidation and adaptive thermoregulation then it can be predicted that PPAR-_amp_#x003b3 agonists could help HD mice to maintain thermoregulatory function when 
18464922PPARPPAR-G2.2The role of PPAR-_amp_#x003b3 in ALS AD and Parkinson's disease are backed with evidence 
18464922PPARPPAR-G2.2with evidence 19 20 38 39 while the role of PPAR-_amp_#x003b3 in HD lacks critical evidence and needs to be studied 
18464922PPARPPAR-G2.2HD and potential neuroprotective role of PGC-1 _amp_#x003b1 in HD PPAR-_amp_#x003b3 desperately seeking further attention and these types of studies could 
18464922PPARPPAR-G2.2of studies could provide essential data on the role of PPAR-_amp_#x003b3 in HD 
18464922PPARPPAR-G2.2Studies in patients treated with PPAR-_amp_#x003b3 agonists indicate that the reduction of insulin resistance is resulted 
18464922PPARPPAR-G2.2reduction of insulin resistance is resulted from the activation of PPAR-_amp_#x003b3 78 
18464922PPARPPAR-G2.2PPAR-_amp_#x003b3 's natural coactivator is PGC-1 _amp_#x003b1 
18464922PPARPPAR-G2.2TZDs can mimic the effect of PGC-1 _amp_#x003b1 on PPAR-_amp_#x003b3 
18464922PPARPPAR-G2.2reduces or become inactivated by acetylation then the activity of PPAR-_amp_#x003b3 could be affected 
18464922PPARPPAR-G2.2In this review we highlighted the role of PPAR-_amp_#x003b3 in neurodegenerative diseases in particular in a mouse model of 
18464922PPARPPAR-G2.2two independent studies provides strong indication for the involvement of PPAR-_amp_#x003b3 in ALS 
18464922PPARPPAR-G2.2Whether PPAR-_amp_#x003b3 is involved in HD remains to be clarified as one 
18464922PPARPPAR-G2.2the treatment of R6/2 R6 2 mice with rosiglitazone another PPAR-_amp_#x003b3 agonist had no beneficial effect 
18464922PPARPPAR-G2.2In the future we will explore the mechanisms by which PPAR-_amp_#x003b3 agonists produce neuroprotection in a mouse model of ALS and 
18464922PPARPPAR-G2.2neuroprotection in a mouse model of ALS and test whether PPAR-_amp_#x003b3 has a role in HD 
18464922PPARPPAR-G2.2be of great interest to determine whether the effect of PPAR-_amp_#x003b3 is powered by glial or neuronal cells or both in 
18464922PPARPPAR-G2.2also be of great interest to determine the effect of PPAR-_amp_#x003b3 agonist on muscles in ALS and HD mouse models 
18464922PPARPPAR-G2.2cell culture studies are necessary in determining the role of PPAR-_amp_#x003b3 in ALS and HD 
18464922PPARPPAR-G2.2it would be very informative to test the effect of PPAR-_amp_#x003b3 agonists on HD mouse models for their effect in thermoregulation 
18464922PPARPPAR-G2.2However since PPAR-_amp_#x003b3 agonist shown to activate PGC-1 _amp_#x003b1 therefore there is an 
18464922PPARPPAR-G2.2is an indirect possibility that PGC-1 _amp_#x003b1 in connection with PPAR-_amp_#x003b3 could play some role in ALS 
18464925PPARPPAR-G2.2Abstract In the recent years the peroxisome proliferator-activated receptor-_amp_#x003b3 PPAR-_amp_#x003b3 a well known target for type II diabetes treatment has 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 agonists which include naturally occurring compounds (such such as long 
18464925PPARPPAR-G2.2The pleiotropic effects of PPAR-_amp_#x003b3 agonists are likely to be mediated by several mechanisms involving 
18464925PPARPPAR-G2.2will review the recent findings supporting a major role for PPAR-_amp_#x003b3 agonists in controlling neuroinflammation and neurodegeneration through their activities on 
18464925PPARPPAR-G2.2The peroxisome proliferator-activated receptor-_amp_#x003b3 PPAR-_amp_#x003b3 belongs to the hormone nuclear receptor super family 
18464925PPARPPAR-G2.2the regulation of genes involved in lipid and carbohydrate metabolism PPAR-_amp_#x003b3 and the other two isoforms PPAR-_amp_#x003b1 and _amp_#x003b4 deeply affect 
18464925PPARPPAR-G2.2accumulating evidence suggests that besides diabetes and metabolic syndrome 4 PPAR-_amp_#x003b3 agonists have significant therapeutic potential in brain disorders 
18464925PPARPPAR-G2.2of experimental studies and few clinical observations have suggested that PPAR-_amp_#x003b3 ligands may be successfully exploited to treat a wide range 
18464925PPARPPAR-G2.2well known model for autoimmune demyelinating diseases synthetic and natural PPAR-_amp_#x003b3 ligands_amp_#x02014 as well as some PPAR-_amp_#x003b1 or _amp_#x003b4 agonists_amp_#x02014 have 
18464925PPARPPAR-G2.2obtained in experimental models of ocular diseases have evidenced that PPAR-_amp_#x003b3 could be targeted to control inflammation and treat invalidating diseases 
18464925PPARPPAR-G2.2The beneficial effects of PPAR-_amp_#x003b3 agonists in degenerative inflammatory and traumatic brain pathologies are most 
18464925PPARPPAR-G2.2Besides microglia PPAR-_amp_#x003b3 agonists can act on other neural cell types including astrocytes 
18464925PPARPPAR-G2.2Several of the beneficial effects of PPAR-_amp_#x003b3 result from its ability once activated by specific ligand to 
18464925PPARPPAR-G2.2In addition some PPAR-_amp_#x003b3 ligands may exert specific activities independently from PPAR-_amp_#x003b3 
18464925PPARPPAR-G2.2addition some PPAR-_amp_#x003b3 ligands may exert specific activities independently from PPAR-_amp_#x003b3 
18464925PPARPPAR-G2.2Figure 1 Cellular targets of PPAR-_amp_#x003b3 agonists in neurodegenerative diseases 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 agonists can control neuroinflammation neurodegeneration and demyelination by effecting several 
18464925PPARPPAR-G2.2Figure 2 PPAR-_amp_#x003b3 expression in culture rat oligodendrocytes and in white matter (postnatal 
18464925PPARPPAR-G2.2rat OL progenitor cultures prepared as previously described 40 for PPAR-_amp_#x003b3 (more more ... 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 STRUCTURE FUNCTIONS AND AGONISTS 
18464925PPARPPAR-G2.2The PPAR-_amp_#x003b3 and the two closely related PPAR-_amp_#x003b1 and PPAR-_amp_#x003b4 (also also 
18464925PPARPPAR-G2.2The PPAR-_amp_#x003b3 and the two closely related PPAR-_amp_#x003b1 and PPAR-_amp_#x003b4 (also also known as _amp_#x003b2 NUC-1 or FAAR share aJunguk Hur
18464925PPARPPAR-G2.2fatty acids such as the liver muscle and heart whereas PPAR-_amp_#x003b4 shows a much wider distributionJunguk Hur
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 is highly expressed in adipose tissue and in cells of 
18464925PPARPPAR-G2.2In the brain PPAR-_amp_#x003b3 is expressed in several cell types including microglia astrocytes oligodendrocytes 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 protein shows a remarkable conservation across species 
18464925PPARPPAR-G2.2Human and the murine PPAR-_amp_#x003b3 proteins show 95% identity at the amino acid level 
18464925PPARPPAR-G2.2The human PPAR-_amp_#x003b3 gene is located on chromosome 3 and generates at least 
18464925PPARPPAR-G2.2on chromosome 3 and generates at least three mRNA transcripts PPAR-_amp_#x003b3 1 PPAR-_amp_#x003b3 2 and PPAR-_amp_#x003b3 3 30 _amp_#x02013 32 
18464925PPARPPAR-G2.23 and generates at least three mRNA transcripts PPAR-_amp_#x003b3 1 PPAR-_amp_#x003b3 2 and PPAR-_amp_#x003b3 3 30 _amp_#x02013 32 
18464925PPARPPAR-G2.2at least three mRNA transcripts PPAR-_amp_#x003b3 1 PPAR-_amp_#x003b3 2 and PPAR-_amp_#x003b3 3 30 _amp_#x02013 32 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 1 e PPAR-_amp_#x003b3 3 mRNAs encode for the same protein 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 1 e PPAR-_amp_#x003b3 3 mRNAs encode for the same protein while PPAR-_amp_#x003b3 2 
18464925PPARPPAR-G2.2e PPAR-_amp_#x003b3 3 mRNAs encode for the same protein while PPAR-_amp_#x003b3 2 mRNA gives rise to a protein containing 28 additional 
18464925PPARPPAR-G2.2Some arachidonic acid metabolites are more effective PPAR-_amp_#x003b3 ligands than the precursor 
18464925PPARPPAR-G2.2_amp_#x003b2 -unsaturated ketone in the cyclopentenone ring was the first PPAR-_amp_#x003b3 endogenous ligand described in 1995 by two independent groups 33 
18464925PPARPPAR-G2.2The implication of PPAR-_amp_#x003b3 in several important metabolic and degenerative disorders has strongly pushed 
18464925PPARPPAR-G2.2and degenerative disorders has strongly pushed the research of specific PPAR-_amp_#x003b3 agonists and antagonist (for for review see 35 
18464925PPARPPAR-G2.2A major group of synthetic PPAR-_amp_#x003b3 agonists is represented by the antidiabetic drugs TZDs originally identified 
18464925PPARPPAR-G2.2A different series of synthetic PPAR-_amp_#x003b3 ligands are derived by L-tyrosine GI262570 GW1929 and GW7845 which 
18464925PPARPPAR-G2.2were developed on the basis of their activity on human PPAR-_amp_#x003b3 and are among the most potent PPAR-_amp_#x003b3 agonists being active 
18464925PPARPPAR-G2.2activity on human PPAR-_amp_#x003b3 and are among the most potent PPAR-_amp_#x003b3 agonists being active at low nanomolar concentrations 
18464925PPARPPAR-G2.2In most cases the doses required for PPAR-_amp_#x003b3 agonist activity are in the high micromolar range thus largely 
18464925PPARPPAR-G2.2flurbiprofen HCT1026 and NXC 2216 were both able to activate PPAR-_amp_#x003b3 and induce its specific binding to a PPRE sequence 36 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 AGONISTS AND OLIGODENDROCYTE BIOLOGY 
18464925PPARPPAR-G2.2myelination 43 44 recent findings support an important role for PPAR-_amp_#x003b3 activators in OL protection and differentiation 
18464925PPARPPAR-G2.2The first evidence for a role of PPAR-_amp_#x003b3 in OL differentiation was reported by Roth et al 45 
18464925PPARPPAR-G2.2all three PPAR isoforms and found that natural and synthetic PPAR-_amp_#x003b3 agonists but not other isoform activators enhance process extension and 
18464925PPARPPAR-G2.2These effects were blocked by the PPAR-_amp_#x003b3 antagonist GW9662 
18464925PPARPPAR-G2.2These observations suggest that PPAR-_amp_#x003b3 mediated mechanisms may be important for OL differentiation and peroxisome 
18464925PPARPPAR-G2.2In line with the proposed role of PPAR-_amp_#x003b3 in controlling OL differentiation and functions we have recently confirmed 
18464925PPARPPAR-G2.2differentiation and functions we have recently confirmed the expression of PPAR-_amp_#x003b3 in highly purified rat OL cultures ( Figure 2 (a)) 
18464925PPARPPAR-G2.2In addition we found an increased expression of PPAR-_amp_#x003b3 in white matter of young rats (post post natal day 
18464925PPARPPAR-G2.2Whether PPAR-_amp_#x003b3 over-expression is part of an adaptive response to the hypoxic 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 AGONISTS AND OLIGODENDROCYTE BIOLOGY 
18464925PPARPPAR-G2.2the above findings Xiang et al 49 reported that the PPAR-_amp_#x003b3 natural ligand 15d-PGJ 2 but not other PGs induced apoptosis 
18464925PPARPPAR-G2.2cultures 50 cell death was independent of the nuclear receptor PPAR-_amp_#x003b3 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 AGONISTS AND ASTROCYTES 
18464925PPARPPAR-G2.2Astrocytes express PPAR-_amp_#x003b3 53 54 and accumulating evidence over the last ten years 
18464925PPARPPAR-G2.2and accumulating evidence over the last ten years indicates that PPAR-_amp_#x003b3 agonists modulate astrocyte functions 
18464925PPARPPAR-G2.2in time- and dose-dependent manners through a mechanism independent of PPAR-_amp_#x003b3 and involving cAMP/PKA cAMP PKA signaling 55 
18464925PPARPPAR-G2.2Another important mechanism by which PPAR-_amp_#x003b3 agonists could exert neuroprotection by influencing astrocyte functions is the 
18464925PPARPPAR-G2.2Romera et al 56 reported that the PPAR-_amp_#x003b3 antagonists T0070907 prevented the ischemic preconditioning-induced (IPC) IPC neuroprotection in 
18464925PPARPPAR-G2.2gene suggesting GLT1/EAAT2 GLT1 EAAT2 glutamate transporter is a novel PPAR-_amp_#x003b3 target gene 56 
18464925PPARPPAR-G2.2Such neurotoxic activities have been shown to be reduced by PPAR-_amp_#x003b3 agonists in several experimental paradigms 
18464925PPARPPAR-G2.2in vivo effects were substantially attenuated by cotreatment with the PPAR-_amp_#x003b3 antagonist GW9662 supporting the involvement of PPAR-_amp_#x003b3 activation 
18464925PPARPPAR-G2.2cotreatment with the PPAR-_amp_#x003b3 antagonist GW9662 supporting the involvement of PPAR-_amp_#x003b3 activation 
18464925PPARPPAR-G2.2Erk Jnk and p38 MAP kinase in astrocytes by a PPAR-_amp_#x003b3 independent mechanism which required the presence of ROS 
18464925PPARPPAR-G2.2Again independently of PPAR-_amp_#x003b3 15d-PGJ 2 and rosiglitazone reduced the phosphorylation of signal transducers 
18464925PPARPPAR-G2.2multiple sclerosis this observation further support the potential role of PPAR-_amp_#x003b3 agonists in MS treatment 5 64 
18464925PPARPPAR-G2.2In line with the beneficial effect of PPAR-_amp_#x003b3 agonists in experimental models of inflammatory diseases PPAR-_amp_#x003b3 has also 
18464925PPARPPAR-G2.2effect of PPAR-_amp_#x003b3 agonists in experimental models of inflammatory diseases PPAR-_amp_#x003b3 has also been involved in anti-inflammatory functions of IL-4 a 
18464925PPARPPAR-G2.2by IL-4 in inflammatory cytokine-stimulated mixed cultures are mediated by PPAR-_amp_#x003b3 activation 
18464925PPARPPAR-G2.2authors describe a coordinate increase in the expression of both PPAR-_amp_#x003b3 and its natural ligand-producing enzyme 12/15-lipoxygenase 12 15-lipoxygenase (12/15-LOX) 12 
18464925PPARPPAR-G2.212 15-LOX in IL-4-treated glial cells and show that IL-4-induced PPAR-_amp_#x003b3 activation antagonizes NF-_amp_#x003ba B transactivation in inflammatory cytokine-stimulated astrocytes 
18464925PPARPPAR-G2.2A similar upregulation of PPAR-_amp_#x003b3 by IL-4 was demonstrated in cultured microglial cells 66 
18464925PPARPPAR-G2.2To link between IL-4 and PPAR-_amp_#x003b3 is completed by the observation that the anti-inflammatory activity of 
18464925PPARPPAR-G2.2the release of proinflammatory mediators induced by Staphylococcus aureus in PPAR-_amp_#x003b3 -deficient astrocytes supporting PPAR-_amp_#x003b3 -independent effects of these compounds 
18464925PPARPPAR-G2.2mediators induced by Staphylococcus aureus in PPAR-_amp_#x003b3 -deficient astrocytes supporting PPAR-_amp_#x003b3 -independent effects of these compounds 
18464925PPARPPAR-G2.2Interestingly OTA increased PPAR-_amp_#x003b3 expression possibly increasing the susceptibility of OTA-exposed cells to PPAR-_amp_#x003b3 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 expression possibly increasing the susceptibility of OTA-exposed cells to PPAR-_amp_#x003b3 agonist treatment 69 
18464925PPARPPAR-G2.2PPAR-_amp_#x003b3 AGONISTS AND MICROGLIAL CELLS 
18464925PPARPPAR-G2.2In this view PPAR-_amp_#x003b3 agonists have been extensively studied in the last decade for 
18464925PPARPPAR-G2.2provided by Petrova et al 74 who demonstrated that this PPAR-_amp_#x003b3 natural ligand attenuates iNOS expression and the subsequent NO accumulation 
18464925PPARPPAR-G2.2was suggested that 15d-PGJ 2 inhibits iNOS expression by a PPAR-_amp_#x003b3 independent mechanism 
18464925PPARPPAR-G2.2first time that primary microglial cells unlike BV-2 cells express PPAR-_amp_#x003b3 and that such basal expression is increased by its specific 
18464925PPARPPAR-G2.2Microglial PPAR-_amp_#x003b3 was subsequently shown to be functionally active being able to 
18464925PPARPPAR-G2.2histocompatibility complex (MHC) MHC class II antigens by mechanisms involving PPAR-_amp_#x003b3 activation and reduced activation of STAT-1 and NF-_amp_#x003ba B which 
18464925PPARPPAR-G2.22 ciglitazone and troglitazone prevented LPS-induced neuronal death suggesting a PPAR-_amp_#x003b3 mediated mechanism of neuroprotection 79 
18464925PPARPPAR-G2.2NXC 2216 were able to prevent microglial activation by activating PPAR-_amp_#x003b3 36 37 
18464925PPARPPAR-G2.2Interestingly NCX 2216 after an initial activation induced PPAR-_amp_#x003b3 nitration and inactivation 
18464925PPARPPAR-G2.2NCX 2216 could therefore lead after an initial activation of PPAR-_amp_#x003b3 to a protracted suppression of its control over microglial activation 
18464925PPARPPAR-G2.2The contribution of PPAR-_amp_#x003b3 -dependent or independent mechanisms to the inhibition of microglial activation 
18464925PPARPPAR-G2.22 at concentrations several fold lower than those required for PPAR-_amp_#x003b3 activation effectively reduced the LPS-stimulated production of PGJ 2 by 
18464925PPARPPAR-G2.2At concentration 10 times higher than those required to activate PPAR-_amp_#x003b3 15d-PGJ 2 induced microglial cell impairment and death by apoptosis 
18464925PPARPPAR-G2.2the link between the proapoptotic effect of 15d-PGJ 2 and PPAR-_amp_#x003b3 activation is still controversial 
18464925PPARPPAR-G2.2and human and rat glioma cell lines appears mediated by PPAR-_amp_#x003b3 -dependent mechanisms 61 87 89 _amp_#x02013 91 
18464925PPARPPAR-G2.2an increasing number of experimental studies supporting the use of PPAR-_amp_#x003b3 ligands to treat major disabling brain diseases with a high 
18464925PPARPPAR-G2.2in animal models of AD due to the ability of PPAR-_amp_#x003b3 agonists to reduced inflammation and the amyloid burden by various 
18464925PPARPPAR-G2.2Similarly the better neurological outcome reported after administration of PPAR-_amp_#x003b3 ligands in experimental stroke models are consistent with the result 
18464925PPARPPAR-G2.2The clinical use of PPAR-_amp_#x003b3 agonists in MS and ASL remains poorly investigated 
18464925PPARPPAR-G2.2Although PPAR-_amp_#x003b3 synthetic ligands such as TZDs and NSAIDs appear to be 
18464925PPARPPAR-G2.2Among these the toxic effect associated with some PPAR-_amp_#x003b3 agonists and their blood-brain-barrier permeability which are at present still 
18464925PPARPPAR-G2.2A deep knowledge of the molecular mechanisms evoked by PPAR-_amp_#x003b3 ligands either dependent or independent of the receptor activation and 
18464925PPARPPAR-G2.2the specific cell type is mandatory for the development of PPAR-_amp_#x003b3 drugs with increasing efficacy and safety 
18513389PPARGPPARG2.2five experiments consisted of peroxisome proliferator activated receptor gamma (PPARG) PPARG pro12ala (chromosome chromosome 3p25 lipoprotein lipase (LPL) LPL asp9asn (chromosome 
15081582peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0another prostaglandin 15 deoxy_amp_#x394; 12 14 pgj 2 a natural peroxisome proliferator activated receptor gamma ligand formed from pgd 2 induces apoptosis in both human astrocytes chattopadhyay et al. 2000 and cortical neurons rohn et al. 2001 .  
15649489peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0we investigated the therapeutic effect of pioglitazone a peroxisome proliferator activated receptor gamma ppar _amp_#x3b3; agonist in the g93a sod1 transgenic mouse model of als.  
15649489peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0in the present studies we tested the neuroprotective effects of the peroxisome proliferator activated receptor gamma agonist pioglitazone.  
16120782ppar gammappar gamma1.0because peroxisome proliferator activated receptor gamma ppar gamma agonists act as potent anti inflammatory drugs we tested whether superoxide dismutase sod1 g93a transgenic mice a mouse model of als benefit from oral treatment with the ppar gamma agonist pioglitazo 
16120782ppar gammappar gamma1.0 agonists act as potent anti inflammatory drugs we tested whether superoxide dismutase sod1 g93a transgenic mice a mouse model of als benefit from oral treatment with the ppar gamma agonist pioglitazone pio .  
16120782peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0because peroxisome proliferator activated receptor gamma ppar gamma agonists act as potent anti inflammatory drugs we tested whether superoxide dismutase sod1 g93a transgenic mice a mouse model of als benefit from oral treatment with the ppar gamma agonist 
16120782ppar gammappar gamma1.0peroxisome proliferator activated receptor gamma ppar gamma ligands were developed as oral antidiabetic drugs after the discovery that ppar gamma activation increases insulin sensitivity and normalizes serum glucose levels berger and moller 2002 gamma activators of the thiazolidinedione tzd class of antidiabetic drugs.  
16120782peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0peroxisome proliferator activated receptor gamma ppar gamma ligands were developed as oral antidiabetic drugs after the discovery that ppar gamma activation increases insulin sensitivity and normalizes serum glucose levels berger and moller 2002 ga 
16120782ppar gammappar gamma1.0beyond their insulin sensitizing and other metabolic actions ppar gamma ligands exert several other ppar gamma dependent and independent antineoplastic and anti inflammatory effects daynes and jones 2002 ; blanquart et al. 2003 ; grommes et al. 2004 .  
16120782ppar gammappar gamma1.0in microglia and macrophages ppar gamma activation results in inhibition of proinflammatory gene expression through various mechanisms landreth and heneka 2001 gamma agonists reduce amyloid beta peptide and cytokine mediated neuroinflammat 
16120782ppar gammappar gamma1.0given the beneficial effects observed in these studies we tested whether an oral treatment of sod1 transgenic mice with the ppar gamma agonist pioglitazone would reduce neuroinflammation protect from motor neuron loss and improve clinical als symptoms.  
16120782ppar gammappar gamma1.0ppar gamma ligands suppress microglial activation thereby protecting neurons from inflammation mediated cell death heneka et al. 1999 ~50%.  
16120782ppar gammappar gamma1.0ppar gamma and neuroinflammation  
16120782ppar gammappar gamma1.0originally developed as oral antidiabetics agonists of ppar gamma have been found to exert potent anti inflammatory effects in several models of neuroinflammation landreth and heneka 2001 gamma mediated reduction of inflammation was neuroprotective we hypothesized  
16120782ppar gammappar gamma1.0s of neuroinflammation landreth and heneka 2001 gamma mediated reduction of inflammation was neuroprotective we hypothesized that sod1 g93a transgenic mice would benefit from chronic treatment with a ppar gamma agonist within the thiazolidinedione class of ppar gamma agonists pio is the only substance that penetrates the blood brain barrier to a significant extent maeshiba et al. 1997 and has therefore been 
16120782ppar gammappar gamma1.0 agonist within the thiazolidinedione class of ppar gamma agonists pio is the only substance that penetrates the blood brain barrier to a significant extent maeshiba et al. 1997 and has therefore been chosen for treatment experiments.  
16120782ppar gammappar gamma1.0ppar gamma and microglial activation  
16120782ppar gammappar gamma1.0ppar gamma mediated inhibition of inflammatory mediators  
16120782ppar gammappar gamma1.0ppar gamma mediated activation of anti inflammatory genes  
16120782ppar gammappar gamma1.0several ppar gamma dependent and independent anti inflammatory actions of the tzd class of drugs have been described and suppression of inflammation may be achieved not at a single but at multiple levels including dire 
16120782ppar gammappar gamma1.0the principal clinical usage of ppar gamma agonists is for treatment of type ii diabetes.  
16120782ppar gammappar gamma1.0it has been shown recently that ppar gamma agonist treatment leads to an upregulation of cu/zn sod1 expression in a rat model of ischemia shimazu et al. 2005 suggesting that enhanced sod1 levels may be protective by reducing oxidative stress. 
16120782ppar gammappar gamma1.0sing an early anti inflammatory treatment strategy initiated well before the first onset of clinical symptoms does not allow us to conclude that patients suffering from sporadic als will benefit from ppar gamma agonist treatment if initiated after clinical onset of disease.  
16120782ppar gammappar gamma1.0however it seems possible that in the case of familiar als family members with an inherited als risk which can be diagnosed before the appearance of clinical symptoms may benefit from prophylactic ppar gamma agonist medication.  
16766086peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0the type ii nuclear receptor peroxisome proliferator activated receptor gamma ppar_amp_#x3b3; has proven to be an attractive target for treatment of cns disease as agonists of this receptor have been shown to be effective in ameliorating disease related symptomology and pathol 
17805244ppar gammappar gamma1.0ppar gamma|pharmaceutical preparations|  
18312546peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0to assess molecular pathological effects of the anti inflammatory peroxisome proliferator activated receptor gamma ppargamma agonist pioglitazone in als we verified changes in the population of neurons astrocytes and microglia in the ventral horns of spinal cord lumbar segments from the pioglitazone treated and n 
18513389peroxisome proliferator activated-receptor gammaperoxisome proliferator activated receptor gamma1.0genetic variants independently selected by four twist procedures the number of genetic variants selected four times over five experiments consisted of: peroxisome proliferator activated receptor gamma pparg pro12ala chromosome 3p25 lipoprotein lipase lpl asp9asn chromosome 8p22 paraoxonase 1 pon1 met55leu and paraoxonase 2 pon2 ser311cys chromosome 7q21.3 tumor necrosis factor beta tnf beta thr26