Figure 3.

Schematic illustrating the role of DSC secretomes modulating the nerve regeneration in CNS. Alzheimer's disease (AD) responds to the production of β-amyloid fibres/plaque which triggers the microglia and astrocytes activation and generation of proinflammatory cytokines. The chronic activation of microglia and astrocytes causes neuron degeneration. Stimulation by GFs and cytokine derived from DSCs secretome such as A2M cytokine is capable of binding to β-amyloid fibres/plaque that mediate the clearance and degradation [1] while FKN can execute their phagocytic functions. In addition, Siglec-9 and MCP-1 can switch the M1 to M2 phenotype for nerve regeneration. This would enhance neuronal plasticity and neurogenesis in AD patients.