Fig. 1
Mitochondrial phenotype of LRRK2G2019S-mutation carriers. Mitochondrial parameters measured in LRRK2G2019S-mutation carriers, without clinical symptoms of PD (NM-LRRK2G2019S) or with clinically manifest PD (PD-LRRK2G2019S) represented as a percentage of decrease/increase when compared to healthy controls, arbitrarily assigned as 0% (black, dotted line) in glucose (blue line) and galactose media (red line). The letters (a), (a’), (b) and (b’), indicate those cases in which a statistical difference within the two analysed groups and controls was found: (a) p < 0.05 when comparing NM-LRRK2G2019S to controls in glucose media, (a’) p < 0.05 when comparing NM-LRRK2G2019S to controls in galactose media, (b) p < 0.05 when comparing PD-LRRK2G2019S to controls in glucose media and (b’) p < 0.05 when comparing PD-LRRK2G2019S to controls in galactose media. In summary, fibroblasts of NM-LRRK2G2019S showed a pattern similar to controls in glucose, except for early disruption of MMP. When subjected to mitochondrial challenging conditions, global mitochondrial function and dynamics trended to ameliorate, towards ATP production (A). Fibroblasts of PD-LRRK2G2019S in glucose trended towards a deranged mitochondrial function when compared to controls. When subjected to galactose media, PD-LRRK2G2019S fibroblasts presented an inefficient increase of mitochondrial function and worsened mitochondrial dynamics, leading to increased oxidative stress (B)