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Study Reveals How the Body Fights off the Damaging Effects of Depression

Update Date: May 23, 2013 10:13 AM EDT

Depression damages the brain and wrecks the body. Previous studies have linked depression with chronic disease and earlier death.  Now a new study may reveal how the body fights off the damaging effects of depression.

Lead investigator Dr. Owen Wolkowitz, professor of psychiatry at UC San Francisco, and his team found that the activity of an enzyme called telomerase is greater in the white blood cells of untreated individuals with major depression. 

Researchers explain that telomerase is an enzyme that lengthens protective end caps on the chromosomes' DNA called telomeres. Telomeres shorten as people age, and previous studies have linked shortened telomeres with earlier death and with chronic diseases in population studies. Other studies have also revealed telomeres shrink more rapidly when people are stressed or depressed.

Researchers explain that the heightened telomerase activity in untreated major depression might represent the body's attempt to fight back against the progression of disease.  The heightened reaction may serve to prevent biological damage in chronically depression individuals.

Researchers also used brain scans to look at the brains of participants.  They found that the size of the hippocampus, a part of the brain responsible for learning and memory, was associated with the amount of telomerase activity measured in the white blood cells.  While the link between hippocampus size and telomerase activity cannot prove a cause-and-effect relationship, researchers said the findings suggest that telomerase helps protect the hippocampus.

Surprisingly, researchers also found that there was a boost in telomerase activity when patients began taking an antidepressant.  The study found that depressed participants with lower telomerase activity and those whose enzyme activity increased the most with treatment showed the greatest improvement in depression symptoms after treatment.

"Our results are consistent with the beneficial effect of telomerase when it is boosted in animal studies, where it has been associated with the growth of new nerve cells in the hippocampus and with antidepressant-like effects, evidenced by increased exploratory behavior," Wolkowitz said in a news release.

The study also looked at telomere length in the same immune cells and found that only very chronically depressed individuals showed telomere shortening.

"The longer people had been depressed, the shorter their telomeres were," Wolkowitz said. "Shortened telomere length has been previously demonstrated in major depression in most, but not all, studies that have examined it. The duration of depression may be a critical factor."

The study involved 20 depressed participants who had been untreated for at least six weeks and had an average lifetime duration of depression of about 13 years and 20 healthy participants who served as controls. Researchers said 16 of the depressed participants were given sertraline, a member of the most popular class of antidepressants, the serotonin-selective-reuptake-inhibitors (SSRIs), and then evaluated again after eight weeks.

Researchers noted that the new findings are preliminary due to the small sample size and must be confirmed through more studies.

Wolkowitz and his team are also looking at how inflammation and oxidative stress affects telomere shortening and accelerated aging in depression.

"New insights into the mechanisms of these processes may well lead to new treatments -- both pharmacological and behavioral -- that will be distinctly different from the current generation of drugs prescribed to treat depression," he said. "Additional studies might lead to simple blood tests that can measure accelerated immune-cell aging."

Researchers plan on presenting their findings t the annual meeting of the American Psychiatric Association in San Francisco.

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