27 June 2013. Some researchers suspect that the debilitating symptoms of schizophrenia emerge from problems with a brain chemical called glutamate. Although glutamate drives much of the electrical signaling between neurons, evidence suggests that in schizophrenia the proteins receiving the glutamate message don’t fully absorb its impact.
A new study published May 31 in the Proceedings of the National Academy of Sciences offers the possibility that D-serine, a simple compound that boosts glutamate signals, can remedy this situation. A team led by Joseph Coyle at Harvard Medical School in Boston, Massachusetts, engineered mice to have underactive glutamate signaling. As adults, these mice exhibited schizophrenia-like features in their brains, including signs that the neurons were less able to adapt themselves to changes around them. Injecting the mice with D-serine for 20 days restored their glutamate signals to normal levels and normalized other markers of a neuron’s ability to change and form connections with other neurons. D-serine also fixed a schizophrenia-like memory problem in these mice.
The results offer hope for treatment because they show that a longstanding, genetically based problem with glutamate may be remedied in adulthood. If the human brain retains a similar response to D-serine in adulthood, this may bode well for clinical trials of compounds that are currently underway. (For more details on this study, see SRF related news story.)—Michele Solis.