Research: Gene Linked to Depression

Research: Gene Linked to Depression

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Ed Yeates ReportingResearchers have more evidence that cells in a certain part of the brain die in people diagnosed with severe depression. In fact, this premature cell death may be the cause of the depression.

In the world of chemistry that bathes our brains for good or ill, scientists at Myriad Genetics have uncovered a gene that may cause depression by signaling too many cells to self-destruct. The discovery supports a theory psychiatric researchers have debated for the past several years.

Research: Gene Linked to Depression

Daniel Christensen, M.D., PhD, Psychiatric Researcher: "There are certain types of cells in certain parts of the brain that would actually degenerate and die in those who had depression. And so, you have enough of them that die and that part of the brain becomes smaller."

Smaller in the part of the brain called the hypocampus. Dr. Daniel Christensen says his colleagues have long known genetics play a major role in depression that is passed down in families. Now, with the discovery of this gene, the biological trigger may become even clearer.

Daniel Christensen, M.D.: "The path of the APAF-1 gene is known to be involved with this signal of when it is a cell dies."

All us experience changes in this part of the brain when we're faced with stressful situations. Most people rebound, but among those with a genetic predisposition for depression, certain forms of this gene overreact, commanding cells to die when they're not ready to die.

Daniel Christensen, M.D.: "If this proves out to be true, it would open a whole new arena of psychopharmacology."

What kind of an arena? Medications, according to Myriad, that would block the action of this rogue protein rather than trying to restore a function that has been lost.

Depression is a group of illnesses that includes depression itself, bi-polar disorders and post-traumatic stress syndrome. They afflict 19 million people in this country or about 10 percent of the population.

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