Experts estimate that approximately three to four percent of Americans will struggle with depression at some point of their lives. Not everyone will receive treatment due to various factors, from cost limitations to lack of social support network.
For those who do seek out treatment, they may encounter some barriers to receiving relief. One of those barriers is the delay usually experienced between the initiation of medication use and the improvement of symptoms.
A recent study conducted by the National Institutes of Health (NIH) shows that there may be a biological marker that can help identify patients who can respond well to a fast-acting antidepressant drug. Not only does the study provide new information that could lead to better treatment options, but the brain signal identified also provides information about the underlying mechanisms related to depression.
The signal, which was viewed by the researchers using noninvasive imaging, is the latest discovery by the NIH team. The team has recently uncovered additional biomarkers, including those detectable in blood and in genetic markers. The current study provided information about ketamine and may be a springboard for the development of personalized therapies.
Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health (NIMH) explained that the information gained can help in focusing the study of molecular targets needed to develop more effective medications. The more specifically the area of the brain related to depression that can be focused on, the more effective the treatment will be, with a reduction in negative side effects.
Zarate, Brian Cornwell, Ph.D. and colleagues based their work on previous research showing that ketamine can effectively alleviate symptoms of depression within hours in some individuals. However, side effects associated with the use of ketamine made it undesirable as a treatment for some people.
The researchers, in work appearing in the journal Biological Psychiatry, examined the mechanism with the goal of developing a safer alternative.
To understand the various effects of ketamine, the NIMH researchers used magnetoencephalography (MEG), imaging the depressed patients’ brains and the electrical activity. The participants were monitored as they rested, when stimulated with the gentle poke of a finger, both before and 6.5 hours following a dose of ketamine.
When certain receptors in the brain were blocked, there was an increase in sporadic electrical signals in the cortex following the dose of ketamine. Within hours of the dose, there was spontaneous electrical activity, whether the drug improved depressive symptoms or the patient experienced no change.
However, it was shown that when poked by a finger, the electrical activity was different in the two groups. Those who responded to ketamine showed a heightened response to the finger stimulation, indicating an increased excitability in the neurons in this particular area of the cortex.
