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New Discovery Sheds Light On Connection Between Traumatic Brain Injuries and Depression

New Discovery Sheds Light On Connection Between Traumatic Brain Injuries and Depression

Over the past ten years, doctors and medical researchers have stepped up efforts to learn more about the ways in which traumatic brain injuries affect patients’ lives. In some cases, the long-term effects of a TBI are not only physical and cognitive but emotional, as well. Recently, researchers from Ohio State University published a study that may explain why some of those who have suffered mild TBIs develop depression later on in life.

The study, published in the journal Biological Psychiatry, compared the brains of mice that had suffered TBIs with the brains of mice that had not. The injured mice exhibited some physical symptoms in the time immediately following their injuries, but each one seemed to fully recover in about a week. After 30 days, researchers examined the brains of the injured mice. They discovered that the injured brains showed signs of continued inflammation caused by a heightened immune response. This inflammation corresponded with depressive symptoms observed in injured mice that were not observed in uninjured mice. The researchers believe that these problems would have worsened over time had they continued to monitor the mice.

In an uninjured brain, cells called microglia act as the primary defenders against infections and injuries by producing inflammation-triggering chemicals. This inflammation is not severe enough to cause damage but rather is just enough to help the brain repair itself. After a brief period, the inflammation subsides.

In injured brains, however, the microglia go on high alert and generate an immune response that causes excessive inflammation. Under these circumstances, even if a patient appears to have recovered fully from a TBI, his brain is damaging itself with its own immune system. In some cases, it may take years before this damage begins to exhibit itself, and it may be the cause of depressive symptoms.

This study is important because it provides essential insight into possible treatments for those with TBI-related emotional issues. First, it may be possible to develop drugs that stop the brain’s natural immune response in the time after an injury, which would reduce inflammation and help prevent long-term damage. Second, knowing that depressive symptoms arise due to an inflammatory response explains why patients with TBI-related depression do not typically respond to antidepressants.

Treatments that prevent or reverse the brain’s immune response are likely years away, but understanding the problem is the first step to helping those who have suffered traumatic brain injuries.