It is not uncommon for individuals with one or more forms of neurodegeneration not to also suffer from depression. These comorbid conditions are especially popular among the aging population. Converging lines of evidence have connected neuroinflammation as a noteworthy contributing factor to both of these ailments. The way to neuroinflammation impacts on neurodegeneration and depression seems to involve alterations in the control and release of pro- and anti-inflammatory cytokines. This can come from an internal or external affront to the system, or from changes in the person because of aging that culminate in immune dysregulation.
Recently, a new study involving a new brain imaging research from the Centre for Addiction and Mental Health (CAMH) reveals that the brain alters after years of persistent depression, suggesting the need to change how we think about depression as it progresses. This study also shows the potential for untreated depression to lead to the development of neuroinflammation in the brain. The study sought to identify the relationship between brain inflammation and depression.
The study involved 80 participants; 25 had untreated depression which had lasted for more than 10 years, 25 for less than 10 years, and 30 had never been diagnosed. All were evaluated with positron emission tomography scans (PET scans) to locate a specific type of protein that results from the brain’s inflammatory response to injury or illness.
The results of the research showed that people with longer and prolonged periods of untreated depression, lasting more than a decade, had significantly more inflammation in their brain compared to those who had less than 10 years of untreated depression.
In an earlier study, Dr. Meyer’s and colleagues were able to discover that the first definitive evidence of inflammation in the brain in clinical depression.
This study is the first of its kind since it provides the first biological evidence for large brain changes in long-lasting depression which might result from untreated depression or depression that is unresponsive to treatment. Hence, the extent of inflammation in the brain can also be used to predict the severity of depression. Hence, it is evident that different stages of depression will require different therapeutics – the same perspective taken for early and later stages of Alzheimer’s disease.
The role of inflammation in disease is now better understood. This was confirmed by senior study author Dr. Jeff Meyer of the Centre for Addiction and Mental Health (CAMH) at the University of Toronto “Greater inflammation in the brain is a common response with degenerative brain diseases as they progress, such as with Alzheimer’s disease and Parkinson’s disease.” Said Dr. Jeff Meyer.
The results of this research and converging lines of evidence suggests that healthcare personnel such as mental health specialists and neuropsychiatrists may need to change their thinking about depression and its effects. The evidence confirms that depression truly is a biologically based disorder of the brain, and left unchecked, it may run a degenerative course that damages brain tissue in ways similar to other neurodegenerative diseases. It is hoped that this finding will lead to the discovery of effective therapies for depression with neuroprotective properties.