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Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies.

Journal of Alzheimer's disease & Parkinsonism

Tong M, Dominguez C, Didsbury J, de la Monte SM.
PMID: 27525190
J Alzheimers Dis Parkinsonism. 2016 Jun;6(3). doi: 10.4172/2161-0460.1000238. Epub 2016 Jun 03.

BACKGROUND: Alzheimer's disease (AD) could be regarded as a brain form of diabetes since insulin resistance and deficiency develop early and progress with severity of neurodegeneration. Preserving insulin's actions in the brain restores function and reduces neurodegeneration. T3D-959 is...

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Tong M, Dominguez C, Didsbury J, et al. Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies. J Alzheimers Dis Parkinsonism. 2016;6(3)doi: 10.4172/2161-0460.1000238.
Tong, M., Dominguez, C., Didsbury, J., & de la Monte, S. M. (2016). Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies. Journal of Alzheimer's disease & Parkinsonism, 6(3), . https://doi.org/10.4172/2161-0460.1000238
Tong, Ming, et al. "Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies." Journal of Alzheimer's disease & Parkinsonism vol. 6,3 (2016). doi: https://doi.org/10.4172/2161-0460.1000238
Tong M, Dominguez C, Didsbury J, de la Monte SM. Targeting Alzheimer's Disease Neuro-Metabolic Dysfunction with a Small Molecule Nuclear Receptor Agonist (T3D-959) Reverses Disease Pathologies. J Alzheimers Dis Parkinsonism. 2016 Jun;6(3). doi: 10.4172/2161-0460.1000238. Epub 2016 Jun 03. PMID: 27525190; PMCID: PMC4979550.
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A PPAR-gamma agonist protects from radiation-induced intestinal toxicity.

United European gastroenterology journal

Mangoni M, Sottili M, Gerini C, Desideri I, Bastida C, Pallotta S, Castiglione F, Bonomo P, Meattini I, Greto D, Cappelli S, Di Brina L, Loi M, Biti G, Livi L.
PMID: 28344789
United European Gastroenterol J. 2017 Mar;5(2):218-226. doi: 10.1177/2050640616640443. Epub 2016 Jul 08.

OBJECTIVE: Because of its anti-inflammatory, anti-fibrotic, anti-apoptotic and anti-neoplastic properties, the PPAR-γ agonist rosiglitazone is an interesting drug for investigating for use in the prevention and treatment of radiation-induced intestinal damage. We aimed to evaluate the radioprotective effect of...

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Mangoni M, Sottili M, Gerini C, et al. A PPAR-gamma agonist protects from radiation-induced intestinal toxicity. United European Gastroenterol J. 2016;5(2):218-226doi: 10.1177/2050640616640443.
Mangoni, M., Sottili, M., Gerini, C., Desideri, I., Bastida, C., Pallotta, S., Castiglione, F., Bonomo, P., Meattini, I., Greto, D., Cappelli, S., Di Brina, L., Loi, M., Biti, G., & Livi, L. (2017). A PPAR-gamma agonist protects from radiation-induced intestinal toxicity. United European gastroenterology journal, 5(2), 218-226. https://doi.org/10.1177/2050640616640443
Mangoni, Monica, et al. "A PPAR-gamma agonist protects from radiation-induced intestinal toxicity." United European gastroenterology journal vol. 5,2 (2017): 218-226. doi: https://doi.org/10.1177/2050640616640443
Mangoni M, Sottili M, Gerini C, Desideri I, Bastida C, Pallotta S, Castiglione F, Bonomo P, Meattini I, Greto D, Cappelli S, Di Brina L, Loi M, Biti G, Livi L. A PPAR-gamma agonist protects from radiation-induced intestinal toxicity. United European Gastroenterol J. 2017 Mar;5(2):218-226. doi: 10.1177/2050640616640443. Epub 2016 Jul 08. PMID: 28344789; PMCID: PMC5349355.
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Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity.

Diabetes & metabolism journal

Corzo C, Griffin PR.
PMID: 24404510
Diabetes Metab J. 2013 Dec;37(6):395-403. doi: 10.4093/dmj.2013.37.6.395.

Adipose tissue, which was once viewed as a simple organ for storage of triglycerides, is now considered an important endocrine organ. Abnormal adipose tissue mass is associated with defects in endocrine and metabolic functions which are the underlying causes...

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Corzo C, Griffin PR. Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity. Diabetes Metab J. 2013;37(6):395-403doi: 10.4093/dmj.2013.37.6.395.
Corzo, C., & Griffin, P. R. (2013). Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity. Diabetes & metabolism journal, 37(6), 395-403. https://doi.org/10.4093/dmj.2013.37.6.395
Corzo, Cesar, and Griffin, Patrick R. "Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity." Diabetes & metabolism journal vol. 37,6 (2013): 395-403. doi: https://doi.org/10.4093/dmj.2013.37.6.395
Corzo C, Griffin PR. Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity. Diabetes Metab J. 2013 Dec;37(6):395-403. doi: 10.4093/dmj.2013.37.6.395. PMID: 24404510; PMCID: PMC3881323.
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Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer.

PPAR research

Lecarpentier Y, Claes V, Vallée A, Hébert JL.
PMID: 28298922
PPAR Res. 2017;2017:5879090. doi: 10.1155/2017/5879090. Epub 2017 Feb 19.

In both colon cancer and type 2 diabetes, metabolic changes induced by upregulation of the Wnt/beta-catenin signaling and downregulation of peroxisome proliferator-activated receptor gamma (PPAR gamma) may help account for the frequent association of these two diseases. In both...

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Lecarpentier Y, Claes V, Vallée A, et al. Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer. PPAR Res. 2017;2017:5879090doi: 10.1155/2017/5879090.
Lecarpentier, Y., Claes, V., Vallée, A., & Hébert, J. L. (2017). Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer. PPAR research, 20175879090. https://doi.org/10.1155/2017/5879090
Lecarpentier, Yves, et al. "Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer." PPAR research vol. 2017 (2017): 5879090. doi: https://doi.org/10.1155/2017/5879090
Lecarpentier Y, Claes V, Vallée A, Hébert JL. Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer. PPAR Res. 2017;2017:5879090. doi: 10.1155/2017/5879090. Epub 2017 Feb 19. PMID: 28298922; PMCID: PMC5337359.
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High-intensity interval training (swimming) significantly improves the adverse metabolism and comorbidities in diet-induced obese mice.

The Journal of sports medicine and physical fitness

Motta VF, Aguila MB, Mandarim-De-Lacerda CA.
PMID: 25665746
J Sports Med Phys Fitness. 2015 Feb 10; Epub 2015 Feb 10.

AIM: Controlling obesity and other comorbidities in the population is a challenge in modern society. High-intensity interval training (HIIT) combines short periods of high-intensity exercise with long recovery periods or a low-intensity exercise. The aim was to assess the...

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Motta VF, Aguila MB, Mandarim-De-Lacerda CA. High-intensity interval training (swimming) significantly improves the adverse metabolism and comorbidities in diet-induced obese mice. J Sports Med Phys Fitness. 2015;
Motta, V. F., Aguila, M. B., & Mandarim-De-Lacerda, C. A. (2015). High-intensity interval training (swimming) significantly improves the adverse metabolism and comorbidities in diet-induced obese mice. The Journal of sports medicine and physical fitness, .
Motta, V F, et al. "High-intensity interval training (swimming) significantly improves the adverse metabolism and comorbidities in diet-induced obese mice." The Journal of sports medicine and physical fitness vol. (2015).
Motta VF, Aguila MB, Mandarim-De-Lacerda CA. High-intensity interval training (swimming) significantly improves the adverse metabolism and comorbidities in diet-induced obese mice. J Sports Med Phys Fitness. 2015 Feb 10; Epub 2015 Feb 10. PMID: 25665746.
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Change of peroxisome proliferator-activated receptor γ expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia.

Anatomy & cell biology

Lee CH, Won MH.
PMID: 24987547
Anat Cell Biol. 2014 Jun;47(2):111-6. doi: 10.5115/acb.2014.47.2.111. Epub 2014 Jun 20.

Peroxisome proliferator-activated receptor γ (PPARγ) has various actions including the regulation of adipocyte differentiation, lipid metabolism and glucose homeostasis. In the present study, we examined the changes of PPARγ immunoreactivity and protein levels in the gerbil dentate gyrus (DG)...

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Lee CH, Won MH. Change of peroxisome proliferator-activated receptor γ expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia. Anat Cell Biol. 2014;47(2):111-6doi: 10.5115/acb.2014.47.2.111.
Lee, C. H., & Won, M. H. (2014). Change of peroxisome proliferator-activated receptor γ expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia. Anatomy & cell biology, 47(2), 111-6. https://doi.org/10.5115/acb.2014.47.2.111
Lee, Choong Hyun, and Won, Moo-Ho. "Change of peroxisome proliferator-activated receptor γ expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia." Anatomy & cell biology vol. 47,2 (2014): 111-6. doi: https://doi.org/10.5115/acb.2014.47.2.111
Lee CH, Won MH. Change of peroxisome proliferator-activated receptor γ expression pattern in the gerbil dentate gyrus after transient global cerebral ischemia. Anat Cell Biol. 2014 Jun;47(2):111-6. doi: 10.5115/acb.2014.47.2.111. Epub 2014 Jun 20. PMID: 24987547; PMCID: PMC4076417.
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Therapy of NAFLD: Insulin Sensitizing Agents.

Journal of clinical gastroenterology

Caldwell SH, Argo CK, Al-Osaimi AM.
PMID: 16672828
J Clin Gastroenterol. 2006 Mar;40:S61-S66. doi: 10.1097/01.mcg.0000168647.71411.48.

Insulin resistance is an integral part of the underlying pathophysiology in most patients with nonalcoholic fatty liver disease (NAFLD). Insulin-sensitiziting agents are therefore likely to be of key importance in the treatment of this disorder, especially in the histologically...

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Caldwell SH, Argo CK, Al-Osaimi AM. Therapy of NAFLD: Insulin Sensitizing Agents. J Clin Gastroenterol. 2006;40:S61-S66doi: 10.1097/01.mcg.0000168647.71411.48.
Caldwell, S. H., Argo, C. K., & Al-Osaimi, A. M. (2006). Therapy of NAFLD: Insulin Sensitizing Agents. Journal of clinical gastroenterology, 40S61-S66. https://doi.org/10.1097/01.mcg.0000168647.71411.48
Caldwell, Stephen H, et al. "Therapy of NAFLD: Insulin Sensitizing Agents." Journal of clinical gastroenterology vol. 40 (2006): S61-S66. doi: https://doi.org/10.1097/01.mcg.0000168647.71411.48
Caldwell SH, Argo CK, Al-Osaimi AM. Therapy of NAFLD: Insulin Sensitizing Agents. J Clin Gastroenterol. 2006 Mar;40:S61-S66. doi: 10.1097/01.mcg.0000168647.71411.48. PMID: 16672828.
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The role of peroxisome proliferator-activated receptors in the development and physiology of gametes and preimplantation embryos.

PPAR research

Huang JC.
PMID: 18354728
PPAR Res. 2008;2008:732303. doi: 10.1155/2008/732303.

In several species, a family of nuclear receptors, the peroxisome proliferator-activated receptors (PPARs) composed of three isotypes, is expressed in somatic cells and germ cells of the ovary as well as the testis. Invalidation of these receptors in mice...

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Huang JC. The role of peroxisome proliferator-activated receptors in the development and physiology of gametes and preimplantation embryos. PPAR Res. 2008;2008:732303doi: 10.1155/2008/732303.
Huang, J. C. (2008). The role of peroxisome proliferator-activated receptors in the development and physiology of gametes and preimplantation embryos. PPAR research, 2008732303. https://doi.org/10.1155/2008/732303
Huang, Jaou-Chen. "The role of peroxisome proliferator-activated receptors in the development and physiology of gametes and preimplantation embryos." PPAR research vol. 2008 (2008): 732303. doi: https://doi.org/10.1155/2008/732303
Huang JC. The role of peroxisome proliferator-activated receptors in the development and physiology of gametes and preimplantation embryos. PPAR Res. 2008;2008:732303. doi: 10.1155/2008/732303. PMID: 18354728; PMCID: PMC2266973.
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PPAR Gamma Activators: Off-Target Against Glioma Cell Migration and Brain Invasion.

PPAR research

Seufert S, Coras R, Tränkle C, Zlotos DP, Blümcke I, Tatenhorst L, Heneka MT, Hahnen E.
PMID: 18815619
PPAR Res. 2008;2008:513943. doi: 10.1155/2008/513943.

Today, there is increasing evidence that PPARgamma agonists, including thiazolidinediones (TDZs) and nonthiazolidinediones, block the motility and invasiveness of glioma cells and other highly migratory tumor entities. However, the mechanism(s) by which PPARgamma activators mediate their antimigratory and anti-invasive...

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Seufert S, Coras R, Tränkle C, et al. PPAR Gamma Activators: Off-Target Against Glioma Cell Migration and Brain Invasion. PPAR Res. 2008;2008:513943doi: 10.1155/2008/513943.
Seufert, S., Coras, R., Tränkle, C., Zlotos, D. P., Blümcke, I., Tatenhorst, L., Heneka, M. T., & Hahnen, E. (2008). PPAR Gamma Activators: Off-Target Against Glioma Cell Migration and Brain Invasion. PPAR research, 2008513943. https://doi.org/10.1155/2008/513943
Seufert, Sebastian, et al. "PPAR Gamma Activators: Off-Target Against Glioma Cell Migration and Brain Invasion." PPAR research vol. 2008 (2008): 513943. doi: https://doi.org/10.1155/2008/513943
Seufert S, Coras R, Tränkle C, Zlotos DP, Blümcke I, Tatenhorst L, Heneka MT, Hahnen E. PPAR Gamma Activators: Off-Target Against Glioma Cell Migration and Brain Invasion. PPAR Res. 2008;2008:513943. doi: 10.1155/2008/513943. PMID: 18815619; PMCID: PMC2542841.
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Mechanisms and clinical effects of thiazolidinediones.

Expert opinion on investigational drugs

Grossman SL, Lessem J.
PMID: 15989661
Expert Opin Investig Drugs. 1997 Aug;6(8):1025-40. doi: 10.1517/13543784.6.8.1025.

Studies of pioglitazone, troglitazone, BRL 49653 and other thiazolidinediones in preclinical animal models of non-insulin dependent diabetes mellitus (NIDDM) and obesity led to the observation that these compounds were effective in reducing hyperglycaemia and hyperlipidaemia. In these models, animals...

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Grossman SL, Lessem J. Mechanisms and clinical effects of thiazolidinediones. Expert Opin Investig Drugs. 1997;6(8):1025-40doi: 10.1517/13543784.6.8.1025.
Grossman, S. L., & Lessem, J. (1997). Mechanisms and clinical effects of thiazolidinediones. Expert opinion on investigational drugs, 6(8), 1025-40. https://doi.org/10.1517/13543784.6.8.1025
Grossman, S L, and Lessem, J. "Mechanisms and clinical effects of thiazolidinediones." Expert opinion on investigational drugs vol. 6,8 (1997): 1025-40. doi: https://doi.org/10.1517/13543784.6.8.1025
Grossman SL, Lessem J. Mechanisms and clinical effects of thiazolidinediones. Expert Opin Investig Drugs. 1997 Aug;6(8):1025-40. doi: 10.1517/13543784.6.8.1025. PMID: 15989661.
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Genetic advances in inflammatory bowel disease.

Current treatment options in gastroenterology

Cho J.
PMID: 16901383
Curr Treat Options Gastroenterol. 2006 Jun;9(3):191-200. doi: 10.1007/s11938-006-0038-z.

The translation of basic science advances to tangible benefits in clinical practice remains a fundamental goal of biomedical research. Genetic approaches provide a unique opportunity to enhance bench-to-bedside translational efforts, with inflammatory bowel disease (IBD) being a model genetic...

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Cho J. Genetic advances in inflammatory bowel disease. Curr Treat Options Gastroenterol. 2006;9(3):191-200doi: 10.1007/s11938-006-0038-z.
Cho, J. (2006). Genetic advances in inflammatory bowel disease. Current treatment options in gastroenterology, 9(3), 191-200. https://doi.org/10.1007/s11938-006-0038-z
Cho, Judy. "Genetic advances in inflammatory bowel disease." Current treatment options in gastroenterology vol. 9,3 (2006): 191-200. doi: https://doi.org/10.1007/s11938-006-0038-z
Cho J. Genetic advances in inflammatory bowel disease. Curr Treat Options Gastroenterol. 2006 Jun;9(3):191-200. doi: 10.1007/s11938-006-0038-z. PMID: 16901383.
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Therapeutic potential of curcumin in non-alcoholic steatohepatitis.

Nutrition research reviews

Shapiro H, Bruck R.
PMID: 19079906
Nutr Res Rev. 2005 Dec;18(2):212-21. doi: 10.1079/NRR2005106.

Non-alcoholic steatohepatitis (NASH) may be associated with a number of clinical conditions, but it occurs most commonly in patients with insulin resistance. There is as yet no established disease-modifying treatment, and a safe and broadly available agent that targets...

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Shapiro H, Bruck R. Therapeutic potential of curcumin in non-alcoholic steatohepatitis. Nutr Res Rev. 2005;18(2):212-21doi: 10.1079/NRR2005106.
Shapiro, H., & Bruck, R. (2005). Therapeutic potential of curcumin in non-alcoholic steatohepatitis. Nutrition research reviews, 18(2), 212-21. https://doi.org/10.1079/NRR2005106
Shapiro, Haim, and Bruck, Rafael. "Therapeutic potential of curcumin in non-alcoholic steatohepatitis." Nutrition research reviews vol. 18,2 (2005): 212-21. doi: https://doi.org/10.1079/NRR2005106
Shapiro H, Bruck R. Therapeutic potential of curcumin in non-alcoholic steatohepatitis. Nutr Res Rev. 2005 Dec;18(2):212-21. doi: 10.1079/NRR2005106. PMID: 19079906.
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Showing 1 to 12 of 240 entries