Genetic Defects, Stress Linked to Abnormal Brain Development

Researchers at Johns Hopkins have uncovered evidence supporting the theory that genetics or stress alone are unlikely to predispose a person to schizophrenia, but the two factors put together—especially when the stress occurs in very early childhood—can raise a person’s risk of developing the disease by as much as one and a half times.

By examining the genomes of thousands of people and comparing them to results from mouse trials, the researchers isolated two chemical compounds long associated with schizophrenia: GABA, a necessary neurotransmitter, and the Disrupted-in-Schizophrenia 1 (DISC1) protein, which helps govern structural brain formation. They then engineered mice to have deficiencies in DISC1, overactive GABA receptors, or both.

The mice with lower DISC1 levels had neural development that appeared similar to normal mice, while those with too much GABA had longer neural appendages than normal. The mice with both modifications had the longest appendages of all, suggesting a synergistic effect between the two chemicals.

Concurrently, a separate team stressed newborn mice by separating them from their mothers for several hours. Normal mice showed no structural changes as a result of the stress, but mice that had lowered DISC1 levels generated neurons that were large and disorganized, including projections that went to the wrong areas of the brain.

To tie their results to human subjects, the two teams analyzed the genomes of 2,961 schizophrenia patients and healthy people for the effects of variations in GABA and DISC1 genes. They found a single genetic sequence that, if present, creates a 140 percent increase in schizophrenia risk, but if the changes occur in only one of the two genes instead of both, there is no corresponding risk.

Source: Cell

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