Communication between the central nervous system and systemic immune responses in Alzheimer’s disease patients. Inflammation clearly occurs in pathologically susceptible regions of the Alzheimer’s disease (AD) brain. Neurodegeneration and neuroinflammation can result in changes of central nervous system (CNS) proteins (for example, amyloid-beta (Aβ) peptide) or inflammatory mediators (acute-phase proteins and pro-inflammatory cytokines and chemokines) across the blood–brain-barrier (BBB). These CNS-derived proteins and mediators may induce systemic immune reactions and/or recruit lymphocytic cells into the CNS. The cells responsible for the inflammatory reaction in CNS are activated microglia and astrocytes. The hypothesis is that Aβ plaques and tangles stimulate a chronic inflammatory reaction. Other than CNS resident cells, blood-derived cells can also be blamed for inflammatory response and seem to accumulate in the AD brain due to the expression of chemokine receptors. The changes in lymphocyte distribution in the AD patient’s blood are also depicted.