p(HGNC:PPARG)
The synthetic TZD PPAR-g agonists are widely prescribed for the treatment of type 2 diabetes mellitus, and have also been shown to be efficacious in a number of CNS disease models [21]. Currently, two TZD agonists, Actos (pioglitazone) and Avandia (rosiglitazone), are FDA approved for the treatment of diabetes. PubMed:21718217
The synthetic TZD PPAR-g agonists are widely prescribed for the treatment of type 2 diabetes mellitus, and have also been shown to be efficacious in a number of CNS disease models [21]. Currently, two TZD agonists, Actos (pioglitazone) and Avandia (rosiglitazone), are FDA approved for the treatment of diabetes. PubMed:21718217
Pedersen and Flynn examined the effects of rosiglitazone and found that activation of PPAR-g ameliorated behavioral deficits in the Tg2576 AD mouse model. However, these animals displayed no changes in plaque pathology, but had reduced brain Ab42 levels. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
Rosiglitazone, a highaffinity agonist for PPARγ, can clear Aβ by activating microglia and promoting its phagocytosis via increasing the levels of CD36, a receptor expressed in it (Escribano et al. 2010) PubMed:29626319
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
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
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. PubMed:21718217
PPAR-g is involved in lipid storage, insulin sensitivity and energy metabolism and has been shown to promote adipocyte differentiation [21]. 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
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
Additionally, PPAR-g can also induce the expression of LXRa creating a metabolically linked cycle. PubMed:21718217
Activation of PPAR-g or PPAR-d has been shown to induce Arg1 and IL-4 expression [105,106]. PubMed:21718217
Activation of PPAR-g or PPAR-d has been shown to induce Arg1 and IL-4 expression [105,106]. 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.