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a(CHEBI:rosiglitazone) increases act(p(HGNC:PPARG)) View Subject | View Object

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

a(CHEBI:rosiglitazone) increases act(p(HGNC:PPARG)) View Subject | View Object

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

a(CHEBI:rosiglitazone) decreases path(MESH:"Diabetes Mellitus, Type 2") View Subject | View Object

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

a(CHEBI:rosiglitazone) increases bp(GO:behavior) View Subject | View Object

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

a(CHEBI:rosiglitazone) causesNoChange a(HBP:HBP00018) View Subject | View Object

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

a(CHEBI:rosiglitazone) decreases a(HBP:HBP00018) View Subject | View Object

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

a(CHEBI:rosiglitazone) decreases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

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

a(CHEBI:rosiglitazone) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

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

a(CHEBI:rosiglitazone) increases bp(GO:"learning or memory") View Subject | View Object

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

a(CHEBI:rosiglitazone) increases p(MGI:Ctnnb1) View Subject | View Object

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

a(CHEBI:rosiglitazone) decreases p(MGI:Gsk3b) View Subject | View Object

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

a(CHEBI:rosiglitazone) increases p(MGI:Abca1) View Subject | View Object

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(CHEBI:rosiglitazone) increases bp(GO:memory) View Subject | View Object

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(CHEBI:rosiglitazone) increases bp(GO:cognition) View Subject | View Object

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(CHEBI:rosiglitazone) increases act(p(HGNC:PPARG)) View Subject | View Object

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

a(CHEBI:rosiglitazone) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

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

a(CHEBI:rosiglitazone) increases act(a(MESH:Microglia)) View Subject | View Object

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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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.