Schizophrenia and major depressive disorder are both caused by perturbations in dopamine signaling. They belong to a group of common psychiatric disorders that are characterized by deficits in motivation and learning. Treatments targeting specific neurotransmitters have been ineffective. However, evidence is emerging that the immune system is a potential therapeutic target.
Granulocyte colony stimulating factor (G-CSF), a cytokine with known neuroprotective properties in the brain, has been shown to inhibit inflammatory proteins such as interleukin-1 and tumor necrosis factor alpha (TNF-alpha).
Recently Erin Calipari, PhD, and colleagues showed that peripheral administration of G-CSF in a mouse model acted directly on dopaminergic circuits to enhance motivation and cognitive flexibility. The authors hypothesized that the effects of G-CSF were a result of its ability to modulate inflammatory signaling, particularly its ability to reduce TNF-alpha expression.
This study, published in the Journal of Neuroscience, suggests that targeting the immune system may provide a new avenue for therapeutic intervention in psychiatric diseases characterized by motivational and cognitive deficits.
This research was supported by Vanderbilt University School of Medicine, the National Intitutes of Health (grants DA042111, DA044308, MH111216) and the Brain and Behavior Research Foundation.
