Additional neurobiological factors that affect both depression and cognition include neuroinflammatory and metabolic changes (46). Specifically, the role of inflammation is an important biological mechanism of cognitive function. This suggestion rests on both the cytokine model of depression (47, 48) and on the the cytokine model of cognitive function that outline the role of cytokines (e.g., TNF-α, IL-6, and IL-1β) in regulating sickness behavior and neurobiological processes subserving cognition, i.e., synaptic plasticity, synaptic scaling, neurogenesis, neurotransmission, and long-term potentiation/depression (LTP/LTD) that are relevant to cognitive function in depression (49). In a recent pilot investigation of CoFaMS, we reported the involvement of B lymphocyte proliferation and ribosomal S26 transcripts specifically in relation to cognitive dysfunction in remitted major depressive disorder (50). Other potential genomic biomarkers of cognitive dysfunction in depression, such as inflammatory and immune, among neurotransmitter and neurotrophic markers require further investigation (51).
