Amyotrophic lateral sclerosis as a protein level, non-genomic disease: Therapy with S2RM exosome released molecules

Figure 1 Differentiation of neural progenitor cells into motor neuron. Once differentiated, only SOD produced by motor neuron. HSP must be supplied to motor neuron from surrounding stem cells. ECM facilitates HSP transfer. SOD: Superoxide dismutase; NPC: Neural progenitor cells; ECM: Extracellular matrix; HSP: Heat shock proteins.

Figure 2 Motor neuron in amyotrophic lateral sclerosis. ALS Motor neurons have misfolded SOD, reduced HSP and mitochondrial function. ALS: Amyotrophic lateral sclerosis; SOD: Superoxide dismutase; SOD1: Superoxide dismutase - misfolded; HSP: Heat shock proteins - disrupted ECM not permissive to HSP transfer; MTC: Mitochondria; ECM: Extracellular matrix.

Figure 3 Repairing motor neurons in amyotrophic lateral sclerosis. SOD, HSP and mitochondrial function are restores to motor neurons. SOD: Superoxide dismutase; SOD1: Superoxide dismutase – misfolded; HSP: Heat shock proteins – disrupted ECM not permissive to HSP transfer; MTC: Mitochondria; NPC: Neural progenitor cells; ECM: Extracellular matrix; FFB: Fetal fibroblast; AC: Fetal astrocyte.

Figure 4 Stimulating and culturing mesenchymal stem cells. TNT formation between stressed and normal MSCs. TNTs facilitate mitochondrial, exosome and molecule transfer between cells. As part of the ECM, the TNTs are extracted with out thermoreversible gel sxtraction procedure, and included in the S2RM. TNT: Tunnelling nanotubes; ECM: Extracellular matrix.

Figure 5 Techniques to capture soluble SRM, exosomes, and self-assembled molecules in extracellular matrix at bottom of culture dish. ECM: Extracellular matrix; MSC: Mesenchymal stem cell.