• Neuroscience · Apr 2015

    Lipoprotein lipase deficiency leads to α-synuclein aggregation and ubiquitin C-terminal hydrolase L1 reduction.

    • H Yang, T Zhou, H Wang, T Liu, K Ueda, R Zhan, L Zhao, Y Tong, X Tian, T Zhang, Y Jin, X Han, Z Li, Y Zhao, X Guo, W Xiao, D Fan, G Liu, and D Chui.
    • Neuroscience Research Institute, Peking University Health Science Center, Beijing 100191, China.
    • Neuroscience. 2015 Apr 2; 290: 1-10.

    AbstractWe 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 α-synuclein (α-syn) and ubiquitin C-terminal hydrolase L1 (UCHL1) are required for normal synaptic and cognitive function. In this study, we found that α-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 α-syn. These results indicated that aggregation of α-syn and reduction of UCHL1 expression in LPL-deficient mice may affect synaptic function. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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