The researchers showed decreasing a set of proteins called Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels reduced depressive behavior in mice. If replicated in humans, the research’s findings could inform new therapies for millions of people with depression who are resistant to existing treatments.
“Drugs currently available for treating depression help most patients, but they stop working for some patients and don’t work from the get-go for others,” said senior author Dr. Dane Chetkovich, a professor of neurology and of physiology at Northwestern University Feinberg School of Medicine. “There is a real need for new therapies to help patients desperate for alternatives to the available therapeutic options.”
Most existing medications for depression affect emotions and mood by increasing levels of some neurotransmitters (serotonin, dopamine and norepinephrine). But the fact that these medications are not effective for many people with depressive disorders suggests there are also other mechanisms underlying depression yet to be uncovered that could be targeted with new therapies.
In future study, the researchers are focusing on adapting the viral gene therapy approach to human patients. They also have a funding from the National Institute of Mental Health to find small molecules that could be developed into oral medications to turn off HCN channels in the brain.
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- Y Han, R J Heuermann, K A Lyman, D Fisher, Q-A Ismail, D M Chetkovich. (2016). HCN-channel dendritic targeting requires bipartite interaction with TRIP8b and regulates antidepressant-like behavioral effects. Molecular Psychiatry.