Fig. 6: Spermine improves lifespan and rescues movement deficits and mitochondrial dysfunction in C.elegans model of PD. | Nature Communications

Fig. 6: Spermine improves lifespan and rescues movement deficits and mitochondrial dysfunction in C.elegans model of PD.

From: Spermine modulation of Alzheimer’s Tau and Parkinson’s α-synuclein: implications for biomolecular condensation and neurodegeneration

Fig. 6

A Schematic overview of C.elegans experiments. B The lifespan of PD C.elegans model of NL5901 treated with control (OP50 vehicle), low (100 µM), medium (200 µM) and high concentration (500 µM) of spermine, which shows that spermine improves the lifespan of PD C.elegans model in a concentration dependent manner. C, D Spermine rescues movement deficits in PD C.elegans model. C bend frequency. (Day10: High SPM vs control, p = 0.0488, Medium SPM vs control, p = 0.0072; Day14: High SPM vs control, p = 0.0189, Medium SPM vs control, p = 0.0075, Low SPM vs control, p = 0.0467). D Head-swing frequency (n = 7), (Day14: High SPM vs control, p = 0.0008, Medium SPM vs control, p < 0.0001, Low SPM vs control, p = 0.0068). E, F Spermine rescues mitochondrial dysfunction in PD C.elegans model of NL5901. Reactive oxygen species (ROS, E), (p < 0.0001). Calcium concentration of mitochondrial (F) (n = 5). (High SPM vs control, p = 0.0087, Medium SPM vs control, p = 0.0091, Low SPM vs control, p = 0.0365). A paired t-test was used. Data are presented as mean values +/− SEM.

Back to article page