Fig. 1

Graphical summary of different mechanisms conducted by MSCs secretome to hippocampal neuron protection. MSC products ameliorate neurodegeneration related to (A1) astrocyte and (M1) microglia, two major immune cells involved in the pathogenesis of Alzheimer’s disease. CX3CL1, IL- 4, IL-13, and IL-10 induced MGs switching from harmful phenotype M1 to protective form M2. Exosomes decrease the expression levels of IL-1a, IL-1β, and TNF-α; thus, MSCs can modulate the excessive inflammatory responses. The elevated secretion of CCL5 and ICAM-1 induces Aβ plaque degradation by increasing the level of protease enzyme (NEP). VEGF and FGF-2 can decrease neuronal apoptosis by changing the BAX/BCL-2 balance in favor of cell survival. IL: interleukin, TGF-β: transforming growth factor-beta, Fractalkine R: fractalkine receptor, TLR: Toll-like receptor, NEP: neprilysin, Aβ: amyloid beta, BAX: BCL-2-associated X, apoptosis regulator, BCL-2: B cell CLL/lymphoma 2. The images depicted in the figure are designed by authors