Beyond Inflammation: Diverse Immune and Metabolic Dysfunctions in Clinical Depression

The role of inflammation in depression grows more complex as additional research is brought to bear on the subject. Not only cytokines and immune dysfunction are involved, but T-cells, macrophages, microglia, and astrocytes may also interact to affect the origins and development of depression, said Bernhard Baune, M.D., Ph.D., at APA’s 2015 annual meeting in Toronto today.

“Chemokines are implicated in various mechanisms and pathways in depression such as pre- and postsynaptic modulation of traditional neurotransmitter systems, regulation of the neuroendocrine axes, control of blood-brain barrier permeability, neuroprotective effects, and regulation of axon sprouting and elongation,” said Baune.

Research by Michael Irwin, M.D., found that sleep disturbance in older adults led to activation of systemic, cellular, and genomic markers of inflammation. That led to depressed mood and anhedonia.

“Sleep disturbance moderates inflammation-induced depression,” reported Irwin. “Experimentally-induced inflammation leads to depression among those who have sleep disturbance but not in those who report minimal sleep complaints.”

Better understanding of the inflammatory and metabolic comorbidity in people with mood disorders could help in developing new therapeutic approaches that target those systems, said Roger McIntyre, M.D. (left).