ArticleDiabetologia2006
Pioglitazone does not increase cerebral glucose utilisation in a murine model of Alzheimer's disease and decreases it in wild-type mice.
Article in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- An evaluation of MSDC-0160, a prototype mTOT modulating insulin sensitizer, in patients with mild Alzheimer's disease.Current Alzheimer research · 2014Trial
- Impact of antidiabetic therapy on cognitive function in patients with type 2 diabetes and Alzheimer's disease: A comprehensive analysis.Journal of Alzheimer's disease : JAD · 2025Article
- Pioglitazone Ameliorates Hippocampal Neurodegeneration, Disturbances in Glucose Metabolism and AKT/mTOR Signaling Pathways in Pentyelenetetrazole-Kindled Mice.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Reassessment of Pioglitazone for Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Relationships between memory decline and the use of metformin or DPP4 inhibitors in people with type 2 diabetes with normal cognition or Alzheimer's disease, and the role APOE carrier status.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- Diabetes and dementia - the two faces of Janus.Archives of medical sciences. Atherosclerotic diseases · 2020Article
- Elevated risk of type 2 diabetes for development of Alzheimer disease: a key role for oxidative stress in brain.Biochimica et biophysica acta · 2014Review
- Intranasal insulin therapy for cognitive impairment and neurodegeneration: current state of the art.Expert opinion on drug delivery · 2013Review
- Hippocampal calcium dysregulation at the nexus of diabetes and brain aging.European journal of pharmacology · 2013Review
- Article
- Imaging of a glucose analog, calcium and NADH in neurons and astrocytes: dynamic responses to depolarization and sensitivity to pioglitazone.Cell calcium · 2011Article
- Neurovascular function in Alzheimer's disease patients and experimental models.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Review
- Intact memory in TGF-β1 transgenic mice featuring chronic cerebrovascular deficit: recovery with pioglitazone.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
- The Nuclear Receptor PPARgamma as a Therapeutic Target for Cerebrovascular and Brain Dysfunction in Alzheimer's Disease.Frontiers in aging neuroscience · 2010Article
- Agonism of Peroxisome Proliferator Receptor-Gamma may have Therapeutic Potential for Neuroinflammation and Parkinson's Disease.Current neuropharmacology · 2007Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisClinical trials are in progress to test thiazolidinediones in neurodegenerative diseases such as Alzheimer's disease that involve deficiencies in brain glucose metabolism. While thiazolidinediones enhance glucose uptake in non-cerebral tissues, their impact on brain energy metabolism has not been investigated in vivo. We thus determined whether the thiazolidinedione pioglitazone reverses the decrease in cerebral glucose utilisation (CGU) in a model of brain metabolic deficiency related to Alzheimer's disease. Results are relevant to diabetes because millions of diabetic patients take pioglitazone as an insulin-sensitising drug, and diabetes increases the risk of developing Alzheimer's disease. MATERIALS AND
methodsThe regional pattern of CGU was measured with the 2-deoxy [(14)C] glucose autoradiographic technique in adult awake mice overexpressing transforming growth factor beta1 (TGFbeta1), and in wild-type littermates. Mice were treated with pioglitazone for 2 months.
resultsMeasurement of CGU in 27 brain regions confirmed that TGFbeta1 overexpression induced hypometabolism across the brain. Pioglitazone did not reverse the effect of TGFbeta1 overexpression and decreased regional CGU in control animals by up to 23%. The extent of the regional CGU decrease induced by pioglitazone, but not that induced by TGFbeta1, correlated strongly with basal CGU, suggesting that the higher the local metabolic rate the greater the reduction of CGU effected by pioglitazone. CONCLUSIONS/
interpretationIn contrast to its stimulatory effect in non-cerebral tissues, chronic treatment with pioglitazone decreases CGU in vivo. This evidence does not support the hypothesis that pioglitazone could act as a metabolic enhancer in Alzheimer's disease, and raises the question of how thiazolidinediones could be beneficial in neurodegenerative diseases.
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