Kelly Jean Thomas

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: Manipulating activity by replacing the kinase domain with a 'kinase-dead' version blocks inclusion body formation and strongly delays cell death, predicting that kinase inhibitors will be useful therapeutic agents in patients with LRRK2 mutations and, perhaps, in sporadic PD.

TL;DR: It is shown that loss of DJ-1 leads to loss of mitochondrial polarization, fragmentation of mitochondria and accumulation of markers of autophagy around mitochondria in human dopaminergic cells, and data suggest thatDJ-1 works in parallel to the PINK1/parkin pathway to maintain mitochondrial function in the presence of an oxidative environment.

TL;DR: The aim of this study was to determine mitochondrial function and morphology in parkin‐mutant patients and to investigate whether pharmacological rescue of impaired mitochondrial function may be possible in Parkin‐Mutant human tissue.

TL;DR: It is shown that L RRK2 predominantly exists as a dimer under native conditions, a state that appears to be stabilized by multiple domain-domain interactions and it is demonstrated that LRRK2 undergoes intramolecular autophosphorylation.