Apolipoprotein E and LRP1 Increase Early in Parkinson's Disease Pathogenesis.
Apolipoprotein E and LRP1 Increase Early in Parkinson's Disease Pathogenesis.
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载脂蛋白 E 和 LRP1 在帕金森病发病机制早期增加。
DOI：
10.1016/j.ajpath.2011.07.021
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Hoozemans,JeroenJM
中科院分区：
文献类型：
--
作者：
Wilhelmus,MichaMM;Bol,JohnGJM;VanHaastert,EliseS;Rozemuller,AnnemiekeJM;Bu,Guojun;Drukarch,Benjamin;Hoozemans,JeroenJM
帕金森病 (PD) 的特征是含有 α-突触核蛋白的路易体 (LB) 和黑质 (SN) 中黑化神经元的丧失。最近，有人提出载脂蛋白 E (ApoE) 表达、α-突触核蛋白聚集和神经变性之间存在联系。在这里，我们报告了 PD 和偶发 LB 疾病病例中 SN 黑色化神经元和 LB 中出现的 ApoE 表达。有趣的是，在偶发的 LB 病和 PD 中也观察到低密度脂蛋白受体相关蛋白 1（ApoE 受体）表达增加。我们的数据表明，SN 黑化神经元脂蛋白稳态/信号传导的改变是 PD 发病机制中的早期事件。
Parkinson's disease (PD) is characterized by α-synuclein–containing Lewy bodies (LBs) and loss of melanized neurons in the substantia nigra (SN). Recently, a link between apolipoprotein E (ApoE) expression, α-synuclein aggregation, and neurodegeneration was suggested. Here, we report on ApoE expression appearing in melanized neurons of the SN and in LBs in both PD and incidental LB disease cases. Interestingly, increased expression of the low-density lipoprotein receptor-related protein 1 (the receptor for ApoE) was also observed in incidental LB disease and PD. Our data suggest that alterations in lipoprotein homeostasis/signaling in melanized neurons of the SN are an early event during PD pathogenesis.