| First Author | Ma D | Year | 2019 |
| Journal | Brain Res | Volume | 1714 |
| Pages | 126-132 | PubMed ID | 30826352 |
| Mgi Jnum | J:281490 | Mgi Id | MGI:6355575 |
| Doi | 10.1016/j.brainres.2019.02.030 | Citation | Ma D, et al. (2019) Long-term liraglutide ameliorates nigrostriatal impairment via regulating AMPK/PGC-1a signaling in diabetic mice. Brain Res 1714:126-132 |
| abstractText | Growing evidence indicates links between type 2 diabetes and Parkinson's disease. The glucagon-like peptide 1 analogue, liraglutide, a commonly used anti-diabetic drug, has protective effects on neurons. The goal of this study was to determine whether long-term liraglutide treatment could reduce the risk of adult type 2 diabetic mice developing Parkinson's disease. Male diabetic db/db mice (12weeks old) were injected daily with liraglutide (n=8), or saline (n=8), and non-diabetic m/m littermates (n=6) were included as controls. Motor function was assessed every 4weeks and all mice were sacrificed after 8weeks of drug intervention for further analysis. The results revealed that long-term treatment of liraglutide protected the db/db mice against the motor function decay and the dopaminergic neuron loss. Liraglutide also restored the impaired AMP kinase (AMPK)/peroxisome proliferator-activated receptor-gamma coactivator 1a (PGC-1a) signaling in the striatum of db/db mice. Further experiments in SH-SY5Y cells supported that AMPK is involved in the neuroprotective effect of liraglutide. In summary, long-term liraglutide ameliorated motor dysfunction and dopaminergic neuron impairment in type 2 diabetic mice, probably via enhancing AMPK/PGC-1a signaling. |
