a(CHEBI:rosiglitazone)
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
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
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
These animals were treated with a low dose of rosiglitazone (3 mg/kg/ day) for 12 weeks and evaluated for plaque deposition and behavior. These animals displayed an approximate 50% decrease in amyloid deposition, a decrease in Ab oligomers, preservation of pre and postsynaptic proteins and the attenuation of cognitive deficits in the Morris water maze. 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
These animals were treated with a low dose of rosiglitazone (3 mg/kg/ day) for 12 weeks and evaluated for plaque deposition and behavior. These animals displayed an approximate 50% decrease in amyloid deposition, a decrease in Ab oligomers, preservation of pre and postsynaptic proteins and the attenuation of cognitive deficits in the Morris water maze. PubMed:21718217
These animals were treated with a low dose of rosiglitazone (3 mg/kg/ day) for 12 weeks and evaluated for plaque deposition and behavior. These animals displayed an approximate 50% decrease in amyloid deposition, a decrease in Ab oligomers, preservation of pre and postsynaptic proteins and the attenuation of cognitive deficits in the Morris water maze. PubMed:21718217
The authors argue that the effects of rosiglitazone were due to the activation of the wnt signaling cascade which they show by an increase in b-catenin expression and a decrease in GSK-3b levels [63]. PubMed:21718217
The authors argue that the effects of rosiglitazone were due to the activation of the wnt signaling cascade which they show by an increase in b-catenin expression and a decrease in GSK-3b levels [63]. PubMed:21718217
While the authors did not detect an increase in ApoE levels in the treated animals, they did observe a modest increase in ABCA1 levels and argue that the enhanced Ab clearance could be attributed to an increase in lipidation of ApoE by ABCA1 [64]. PubMed:21718217
A Phase II clinical trial in which patients were treated with rosiglitazone for 6 months showed improvements in attention and memory retention, but only in patients who did not have an APOE4 allele. PubMed:21718217
A Phase II clinical trial in which patients were treated with rosiglitazone for 6 months showed improvements in attention and memory retention, but only in patients who did not have an APOE4 allele. 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
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
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
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