However, long-term systemic inflammation has been suggested as a plausible explanation, supported by the association of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and other chemokines with both RA and depression.29 These cytokines cross the blood-brain barrier, interacting with the brain and triggering microglial activation, releasing proinflammatory factors.30,31,32 Neural pathways also transmit peripheral inflammation signals to the central nervous system (CNS), inducing CNS inflammation. Here, IL1B is linked to rheumatoid arthritis.