| First Author | Yang H | Year | 2015 |
| Journal | Neuroscience | Volume | 290 |
| Pages | 1-10 | PubMed ID | 25595992 |
| Mgi Jnum | J:221431 | Mgi Id | MGI:5639163 |
| Doi | 10.1016/j.neuroscience.2014.12.068 | Citation | Yang H, et al. (2015) Lipoprotein lipase deficiency leads to alpha-synuclein aggregation and ubiquitin C-terminal hydrolase L1 reduction. Neuroscience 290:1-10 |
| abstractText | We have previously reported that presynaptic dysfunction and cognitive decline have been found in lipoprotein lipase (LPL) deficient mice, but the mechanism remains to be elucidated. Accumulating evidence supported that alpha-synuclein (alpha-syn) and ubiquitin C-terminal hydrolase L1 (UCHL1) are required for normal synaptic and cognitive function. In this study, we found that alpha-syn aggregated and the expression of UCHL1 decreased in the brain of LPL deficient mice. Reduction of UCHL1 was resulted from nuclear retention of DNA cytosine-5-methyltransferase 1 in LPL knockout mice. Reverse changes were found in cultured cells overexpressing LPL. Furthermore, deficiency of LPL increased ubiquitination of alpha-syn. These results indicated that aggregation of alpha-syn and reduction of UCHL1 expression in LPL-deficient mice may affect synaptic function. |
