MOESM5 of Exhaustion of mitochondrial and autophagic reserve may contribute to the development of LRRK2 G2019S -Parkinson’s disease Diana Juárez-Flores Ingrid González-Casacuberta Mario Ezquerra María Bañó Francesc Carmona-Pontaque Marc Catalán-García Mariona Guitart-Mampel Juan Rivero Ester Tobias Jose Milisenda Eduard Tolosa Maria Marti Ruben Fernández-Santiago Francesc Cardellach Constanza Morén Glòria Garrabou 10.6084/m9.figshare.6465374.v1 https://springernature.figshare.com/articles/journal_contribution/MOESM5_of_Exhaustion_of_mitochondrial_and_autophagic_reserve_may_contribute_to_the_development_of_LRRK2___G2019S__-Parkinson_s_disease/6465374 Additional file 5: Figure S2. Genetics and mitochondrial protein synthesis. Results are represented by means ± SEM, comparing controls (white bars), non-manifesting carriers of LRRK2 G2019S -mutation, (NM-LRRK2 G2019S , grey bars) and patients with LRRK2 G2019S -mutation and clinically manifest PD (PD-LRRK2 G2019S , black bars) in glucose and galactose media. A. Mitochondrial DNA was conserved in both groups and media. B. Mitochondrial RNA levels were significantly decreased in NM-LRRK2 G2019S when compared to controls in galactose media C-E. Cell growth, mitochondrial content and protein synthesis did not show differences between groups, in either condition. F. Representative image of Western Blot of mitochondrial proteins in either glucose (Glu) or galactose (Gal) media of the three cohorts studied, the original Blott has been cropped for its better visualization, complete images can be provided at request. 2018-06-08 05:00:00 Parkinson’s disease LRRK2 G2019S Non-manifesting carriers Mitochondrial dysfunction Mitochondrial dynamics Autophagy Fibroblasts Glucose Galactose