Brain atrophy causes depression in multiple sclerosis patients

WASHINGTON - Brain atrophy of a part of brain is what causes depression in people suffering from multiple sclerosis (MS), according to a UCLA study.

Researchers said that atrophy of a specific region of the hippocampus, a critical part of the brain involved in mood and memory, leads to depression among MS patients.

In the first such study in living humans, senior study author Dr. Nancy Sicotte, Stefan Gold, and colleagues used high-resolution magnetic resonance imaging to identify three key sub-regions of the hippocampus that were found to be smaller in people with MS when compared with the brains of healthy individuals.

The researchers also found a relationship between this atrophy and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, a complex set of interactions among three glands.

The HPA axis is part of the neuroendocrine system that controls reactions to stress and regulates many physiological processes.

It is believed that this dysregulation may play a role in the atrophy of the hippocampus and the development of depression.

“Depression is one of the most common symptoms in patients with multiple sclerosis. It impacts cognitive function, quality of life, work performance and treatment compliance. Worst of all, it’s also one of the strongest predictors of suicide,” said Gold.

The researchers examined three sub-regions of the hippocampus region- CA1, CA3 and the dentate gyrus area of the hippocampal region called CA23DG (CA stands for cornu ammonis).

They imaged 29 patients with relapsing remitting multiple sclerosis and compared them with 20 healthy control subjects who did not have MS.

They also measured participants’ cortisol level three times a day.

Cortisol is a major stress hormone produced by the HPA axis that affects many tissues in the body, including the brain.

In addition to the difference between MS patients and healthy controls, the researchers found that the multiple sclerosis patients diagnosed with depression showed a smaller CA23DG sub-region of the hippocampus, along with excessive release of cortisol from the HPA axis.

“Interestingly, this idea of a link between excessive activity of the HPA axis and reduced brain volume in the hippocampus hasn’t received a lot of attention, despite the fact that the most consistently reproduced findings in psychiatric patients with depression (but without MS) include hyperactivity of the HPA axis and smaller volumes of the hippocampus,” said Sicotte.

“So the next step is to compare MS patients with depression to psychiatric patients with depression to see how the disease progresses in each,” she added.

The study was published in the early online edition of the journal Biological Psychiatry. (ANI)