Mechanism by which the pathogenesis of Parkinson's disease is stimulated by Gaucher's mutation.

我们观察到α-突触核蛋白（αS）和P123 β-突触核蛋白（βS）转基因小鼠都有轴突球形成。αS-和P123 H β S-球的溶酶体病理学观察结果相似，而氧化应激与α S-球相关，与P123 H β S-球相关程度较低。其他病理学，如线粒体改变和LRRK 2蓄积，仅在α S球中检测到。总的来说，αS-和P123 H β S-小球通过相似但不同的致病机制形成。

We observed that axonal globules are formed in both αsynuclein (αS)- and P123H Βsynuclein (βS) transgenic mice. Lysosomal pathology was similarly observed for both αS- and P123H βS-globules, while oxidative stress was associated with the αS-globules, and to a lesser extent with the P123H βS-globules. Other pathologies, such as mitochondrial alteration and LRRK2 accumulation, were exclusively detected for αS-globules. Collectively, both αS- and P123H βS-globules were formed through similar but distinct pathogenic mechanisms.