[en] Sir,
In their letter in this issue, Gaare and colleagues (2018) state that TRAP1 may not be a Parkinson’s disease gene because of lack of genetic association. In response, we welcome their data analyses and we welcome any further genetic analyses of TRAP1 variants in additional Parkinson’s disease genetic datasets, including the reanalysis of open access datasets such as the Parkinson’s Progressive Markers Initiative (PPMI). Our point of view is that TRAP1 is an interesting effector protein that our study unequivocally showed is relevant to Parkinson’s disease signaling in the context of mitochondrial regulation. Furthermore, the overall contribution of TRAP1 genetic variants to Parkinson’s disease was not the focus of our recent paper in Brain (Fitzgerald et al., 2017).
Centre de recherche :
- Luxembourg Centre for Systems Biomedicine (LCSB): Clinical & Experimental Neuroscience (Krüger Group) - Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) ULHPC - University of Luxembourg: High Performance Computing
Disciplines :
Génétique & processus génétiques Neurologie
Auteur, co-auteur :
Fitzgerald, Julia C.
Zimprich, Alexander
BOBBILI, Dheeraj Reddy ; University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB)
Sharma, Manu
MAY, Patrick ; University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB)
KRÜGER, Rejko ; University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit
Co-auteurs externes :
yes
Langue du document :
Anglais
Titre :
Reply: No evidence for rare TRAP1 mutations influencing the risk of idiopathic Parkinson’s disease