Fig. 6: C/C cohesion deficits in lymphocytes from R1441G-LRRK2 and G2019S-LRRK2 mutation carriers. | npj Parkinson's Disease

Fig. 6: C/C cohesion deficits in lymphocytes from R1441G-LRRK2 and G2019S-LRRK2 mutation carriers.

From: A potential patient stratification biomarker for Parkinson´s disease based on LRRK2 kinase-mediated centrosomal alterations in peripheral blood-derived cells

Fig. 6: C/C cohesion deficits in lymphocytes from R1441G-LRRK2 and G2019S-LRRK2 mutation carriers.

a Example of healthy control (ctrl) and R1441G-LRRK2 PD lymphocytes from PBMC preparations stained for pericentrin and DAPI. White arrows point to pericentrin-positive structures and yellow arrows to two pericentrin-positive structures displaying a split phenotype. Scale bar, 5 μm. b The C/C splitting phenotype was quantified from 150–200 cells from 10 control, 12 R1441G-LRRK2 PD, 9 R1441G-LRRK2 NMC, 7 G2019S-LRRK2 PD, 6 G2019S-LRRK2 NMC and 4 idiopathic PD patients in either the absence or presence of MLi2 (200 nM, 30 min) as indicated. Bars represent mean ± s.e.m.; ctrl versus R1441G mutation (p < 0.0001); ctrl versus R1441G NMC (p < 0.0001); ctrl versus G2019S mutation (p < 0.0001); ctrl vrsus G2019S NMC (p < 0.0001); ctrl versus idiopathic PD (p < 0.0001); R1441G mutation versus R1441G mutation + MLi2 (p < 0.0001); R1441G NMC versus R1441G NMC + MLi2 (p < 0.0001); G2019S mutation versus G2019S mutation + MLi2 (p < 0.0001); G2019S NMC versus G2019S NMC + MLi2 (p = 0.0001); idiopathic PD versus idiopathic PD + MLi2 (p = 0.006). ****p < 0.001; **p < 0.01. c Paired t-test analysis of C/C cohesion deficits from each cell line in the absence or presence of MLi2 as indicated.

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