p(HGNC:NR1H3)
Importantly, this study utilized the LXR agonist, GW3965, to activate the LXRs and induce the expression of both ApoE and ABCA1. PubMed:21718217
Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
Additionally, PPAR-g can also induce the expression of LXRa creating a metabolically linked cycle. PubMed:21718217
In the past decade, drugs targeting the NRs, peroxisome proliferator-activated receptor g (PPARg) and liver X receptor (LXR) have shown to ameliorate pathogenesis in animal models of AD. PubMed:21718217
Recently, they have been shown to promote the degradation of the Ab peptides in the brain by activating genes responsible for reverse cholesterol transport [13]. PubMed:21718217
LXR activation increased the ApoE particle size of all human ApoE isoforms, suggesting that activation of this pathways may enhance Ab clearance regardless of the ApoE allele expressed [13]. PubMed:21718217
Recently, they have been shown to promote the degradation of the Ab peptides in the brain by activating genes responsible for reverse cholesterol transport [13]. PubMed:21718217
Activation of these receptors has been shown to suppress microglial-mediated inflammatory responses both in vitro and in vivo. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217
Numerous studies have shown that both PPAR-g and LXRs induce the expression of ApoE and ABCA1 and it is through the expression of these proteins that they exert their effects on amyloid pathology. PubMed:21718217
LXR activation increased the ApoE particle size of all human ApoE isoforms, suggesting that activation of this pathways may enhance Ab clearance regardless of the ApoE allele expressed [13]. PubMed:21718217
Numerous studies have shown that both PPAR-g and LXRs induce the expression of ApoE and ABCA1 and it is through the expression of these proteins that they exert their effects on amyloid pathology. PubMed:21718217
A different result was reported by Vanmierlo et al. who found that LXR agonist treatment resulted in restoration of memory, but did not find a change in plaque burden [48]. PubMed:21718217
Indeed, treatment of AD mouse models with LXR or PPAR agonists has resulted in the suppression of microglial activation [44,45,47,59,63]. PubMed:21718217
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.