| First Author | Ruggiero A | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 44401 | PubMed ID | 28276496 |
| Mgi Jnum | J:271556 | Mgi Id | MGI:6281792 |
| Doi | 10.1038/srep44401 | Citation | Ruggiero A, et al. (2017) Loss of forebrain MTCH2 decreases mitochondria motility and calcium handling and impairs hippocampal-dependent cognitive functions. Sci Rep 7:44401 |
| abstractText | Mitochondrial Carrier Homolog 2 (MTCH2) is a novel regulator of mitochondria metabolism, which was recently associated with Alzheimer's disease. Here we demonstrate that deletion of forebrain MTCH2 increases mitochondria and whole-body energy metabolism, increases locomotor activity, but impairs motor coordination and balance. Importantly, mice deficient in forebrain MTCH2 display a deficit in hippocampus-dependent cognitive functions, including spatial memory, long term potentiation (LTP) and rates of spontaneous excitatory synaptic currents. Moreover, MTCH2-deficient hippocampal neurons display a deficit in mitochondria motility and calcium handling. Thus, MTCH2 is a critical player in neuronal cell biology, controlling mitochondria metabolism, motility and calcium buffering to regulate hippocampal-dependent cognitive functions. |
