8/14/2012

Researchers find reasons of brain’s shrink in depression



Studies have revealed that in depression, a part of the brain shrinks.

Certain brain regions in people with major depression are smaller and less dense than those of their healthy counterparts. Now, researchers have traced the genetic reasons for this shrinkage.

A series of genes linked to the function of synapses, or the gaps between brain cells crucial for cell-to-cell communication, can be controlled by a single genetic "switch" that appears to be overproduced in the brains of people with depression, a new study finds.

"We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated," study researcher Ronald Duman, a professor of psychiatry at Yale University, said in a statement.

Transcription factors are proteins that help control which genetic instructions from DNA will be copied, or transcribed, as part of the process of building the body s proteins.

Shrinking brain

Brain-imaging studies, post-mortem examinations of human brains and animal studies have all found that in depression, a part of the brain called the dorsolateral prefrontal cortex shrinks. The neurons in this region, which is responsible for complex tasks from memory and sensory integration to the planning of actions, are also smaller and less dense in depressed people compared with healthy people.

Duman and his colleagues suspected that these neuronal abnormalities would include problems with the synapses, the points where brain cells "talk" to one another. At synapses, neurons release neurotransmitters that are picked up by their neighbors, carrying signals from cell to cell at rapid speed.

The researchers conducted gene profiling on the postmortem brain tissue of both depressed and mentally healthy subjects. They found a range of genes that were significantly less active in depressed people s dorsolateral prefrontal cortexes, particularly five related to synaptic function: synapsin 1, Rab3A, calmodulin 2, Rab4B and TUBB4.

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