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Additional file 2: Table S1. Clinical characteristics of PD-LRRK2 G2019S patients (n=7). The following legend accompanies the table: NM-LRRK2 G2019S : Non-manifesting carriers of LRRK2 G2019S -mutation; PD-LRRK2 G2019S : patients with LRRK2 G2019S -mutation and clinically manifest PD

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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

MOESM1 of Exhaustion of mitochondrial and autophagic reserve may contribute to the development of LRRK2 G2019S -Parkinson’s disease

Additional file 1: Materials and methods. This part of additional material is provided in a separate word document named “Additional material, materials and methods”

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Additional file 4: Table S2. Raw data of mitochondrial phenotype and autophagic print parameters. The following legend accompanies the table: Glu: glucose; Gal: galactose; NM-LRRK2 G2019S : Non-manifesting carriers of LRRK2 G2019S -mutation; PD- LRRK2 G2019S : patients with LRRK2 G2019S -mutation and clinically manifest PD; mtDNA: Mitochondrial DNA; mtRNA: Mitochondrial RNA; CI: Complex I; O2 consumption stimulated for CI: Oxygen consumption stimulated for Complex I substrates (pyruvate, malate and glutamate); CIV: Complex IV. Pa. P value when comparing NM-LRRK2 G2019S vs. controls; Pb. P value when comparing PD- LRRK2 G2019S vs. controls; Pc. P value when comparing NM-LRRK2 G2019S vs. PD-LRRK2 G2019S

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Additional file 3: Figure S1. Principal component analysis (PCA) for patients and controls in the different media. Variables factor map showing that individual variability in glucose media (A) was best expressed by mitochondrial dynamics parameters -circularity and mitochondrial network- for component 1 (horizontal axis), and autophagy parameters for component 2 (vertical axis). When subjected to mitochondrial challenging conditions (B), circularity expressed the greatest variability for component 1 (horizontal axis), and MMP better expressed component 2 variability (vertical axis). The longer vectors and those which are more aligned to the corresponding axis (depicted as dotted lines) are the ones with the greatest variability among individuals, which interestingly have been documented to be associated with PD, despite none of the parameters represent a greater variability between groups. MtDNA: mitochondrial-DNA; mtRNA: mitochondrial-RNAVDAC/βactin: Mitochondrial content; COXII/βactin: Mitochondrial encoded protein content COXIV/βactin; Nuclear encoded protein content; CI: Complex I enzymatic function; PMox: oxygen consumption stimulated by pyruvate-malate; CIV: Complex IV enzymatic function; MMP: Mitochondrial membrane potential; OE: Oxidative stress; Circ: Circularity; P62: Autophagy substrate LC3BI: Autophagy receptor, basal form; LC3BII: Lipidated form of the autophagy receptor, LC3BII/LC3BI: autophagic turnover, LC3BII/P62: autophagic flux