Liliane Glauser

TL;DR: This study demonstrates that expression of G2019S mutant LRRK2 induces the degeneration of nigrostriatal pathway dopaminergic neurons in an age-dependent manner, and will provide important tools for understanding the mechanism(s) through which familial mutations precipitate neuronal degeneration and PD.

TL;DR: Parkin interacts with and selectively mediates the atypical polyubiquitination of the mitochondrial fusion factor, mitofusin 1, leading to its enhanced turnover by proteasomal degradation as mentioned in this paper.

TL;DR: A number of intriguing neuronal phenotypes due to the loss- or gain-of-function of ATP13A2 that support a role for this protein in regulating intracellular cation homeostasis and neuronal integrity are revealed.

TL;DR: A novel functional interaction is identified between LRRK2 and ADP-ribosylation factor GTPase-activating protein 1 (ArfGAP1) and this role may represent a promising target for interfering with L RRK2-dependent neurodegeneration in familial and sporadic PD.

TL;DR: It is established that dominant V PS35 mutations lead to neurodegeneration in PD consistent with a gain-of-function mechanism, and support a key role for VPS35 in the development of PD.