While inflammation triggered by the immune system is a vital response in many cases like when pathogens invade the body, inflammation at the wrong time or too much inflammation can cause problems. Inflammation has even been identified as a potential cause of depression, and scientists from the Emory School of Medicine recently showed locating these inflammatory markers in the brain could lead them to new drug targets for certain cases of depression.
Elevated glutamate levels in the basal ganglia, an area of the brain devoted to motor control, motivation, and decision making, was found to be associated with depressed patients who also have systemic inflammation (
Neuroscience Online). Based on this association, Emory researchers aimed to identify which depression patients would respond best to medication targeting high levels of glutamate in their new study published in
Molecular Psychiatry.
Glutamate is the “major excitatory transmitter” in the brain, but at too-high levels it can be toxic to neurons and glia, which are needed for healthy brain function (
The Neurotransporter Group). This particular study focused on glutamate levels in the basal ganglia after previous studies discovered that hepatitis C treatments stimulated inflammation, depressive symptoms, and increased glutamate in the basal ganglia.
“Inflammation markers can guide us to which depressed patients respond best to glutamate blockers," lead author Ebrahim Haroon, MD, said about the study. "This could be an important step toward personalizing treatment for depression."
Haroon and his team looked at 50 patients with depression not currently receiving antidepressant treatment. They looked for C-reactive protein (CRP) prevalence in the blood stream, a marker of inflammation since protein levels, produced by the liver, rise when there is inflammation in the body (
MedlinePlus). They also measured glutamate levels in the basal ganglia using magnetic resonance spectroscopy (MRS) and myo-inositol, a marker for glial health.
Indeed, their results showed slow motor function, measured by finger tapping speed, and anhedonia, the inability to feel pleasure and a common characteristic of depression, coincided with high levels of glutamate and myo-inositol in the basal ganglia.
This study provides new insight into how individualizing depression treatments can make controlling and limiting the disease much easier. The next challenge for researchers devoted to the connection between inflammation, glutamate, and depression will be to reduce depression-causing inflammation without dampening the power of the immune system to fight disease.
For more on treating depression in patients with high levels of glutamate, check out the following video.
Source:
Emory Health Sciences
