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

@article{Yang2015LipoproteinLD,
  title={Lipoprotein lipase deficiency leads to α-synuclein aggregation and ubiquitin C-terminal hydrolase L1 reduction.},
  author={Huan Yang and Ting Zhou and H Wang and Tong-tong Liu and Kouhei Ueda and Rui Zhan and Linnan Zhao and Yawei Tong and Xiaosheng Tian and Tiejun Zhang and Yichen Jin and Xuemei Han and Zheng Li and Ying Zhao and Xinhu Guo and Weizhong Xiao and Dongsheng Fan and Guozhen Liu and Dehua Chui},
  journal={Neuroscience},
  year={2015},
  volume={290},
  pages={1-10}
}
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 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… CONTINUE READING