Fig. 1

Three-party cross-talk among neurons, microglia and astrocytes in AD. Microglia and astrocytes actively respond to changes in the environment caused by amyloid (Aβ) depositions. Glia change their morphology and function, release neurotransmitters, immunomodulators such as cytokines, chemokines, complement factors and modulate each other’s activity as well as activity of other cells in the environment. Evident communication in AD is mediated by the neuronal Aβ-astrocytic C3/C3a–microglial C3aR axis. Some molecules and receptors as well as some genes and molecular pathways participating in the pathogenesis of the disease are shown. ADE astrocyte-derived exosomes, GDNF glial-derived neurotrophic factor, RAGE receptor for advanced glycation end products, sTREM soluble triggering receptor expressed on myeloid cells