Metformin therapy in a transgenic mouse model of Huntington's disease
| Autor: | Thong C. Ma, Jessica L. Buescher, Benjamin Oatis, Jason A. Funk, Andrew J. Nash, Raeann L. Carrier, Kari R. Hoyt |
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| Rok vydání: | 2007 |
| Předmět: |
Blood Glucose
Male Genetically modified mouse medicine.medical_specialty Huntingtin Glutamine Mice Transgenic AMP-Activated Protein Kinases Motor Activity Protein Serine-Threonine Kinases Central nervous system disease Mice Sex Factors Trinucleotide Repeats Huntington's disease Multienzyme Complexes Internal medicine medicine Animals Hypoglycemic Agents Behavior Animal Dose-Response Relationship Drug business.industry General Neuroscience Neurodegeneration Age Factors medicine.disease Metformin Enzyme Activation Disease Models Animal Dose–response relationship Huntington Disease Endocrinology Female business medicine.drug |
| Zdroj: | Neuroscience Letters. 411:98-103 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/j.neulet.2006.10.039 |
| Popis: | Huntington's disease (HD) is a hereditary neurodegenerative disease that leads to striatal degeneration and a severe movement disorder. We used a transgenic mouse model of HD (the R6/2 line with approximately 150 glutamine repeats) to test a new therapy for this disease. We treated HD mice with metformin, a widely used anti-diabetes drug, in the drinking water (0, 2 or 5mg/ml) starting at 5 weeks of age. Metformin treatment significantly prolonged the survival time of male HD mice at the 2mg/ml dose (20.1% increase in lifespan) without affecting fasting blood glucose levels. This dose of metformin also decreased hind limb clasping time in 11-week-old mice. The higher dose did not prolong survival, and neither dose of metformin was effective in female HD mice. Collectively, our results suggest that metformin may be worth further investigation in additional HD models. |
| Databáze: | OpenAIRE |
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