MORE than 350 million people are affected by depression, making it one of the most common disorders in the world. It is the biggest cause of disability, and as many as two-thirds of those who commit suicide have the condition.
The title of developmental biologist Lewis Wolpert’s book captures the nature of depression: Malignant sadness.
The word “malignant” inadvertently highlights a worrying contrast between advances in cancer research compared to depression research. This is not entirely due to the higher funding of cancer research but also to the technology required to probe depression. These methods are only now becoming available. A key difficulty has been advancing effective treatments. The essential basis of antidepressant pharmacology has not really changed over the last 50 years.
Drug development is a new focus, and there are two main schools of thought on how best to achieve this:
1) So-called “reverse translation”, teasing apart molecular mechanisms in existing effective treatments leading to development of improved compounds.
2) Targeting specific brain circuits that mediate symptoms of mental illness.
A more radical approach has been to target the immune system. The initial link between the immune system and psychiatric and neurodegenerative disorders has been established by a number of studies; these indicate that increased levels of biological markers for inflammatory processes are found in patients with depression and also in Alzheimer’s disease. It has also been shown that inflammatory processes can trigger phenomena that resemble mood disorders or neurodegeneration. But whether anti-inflammatory medicines could benefit patients remains unclear.
A recently formed consortium of UK scientists and researchers from two pharmaceutical companies is investigating whether mood disorders, such as depression, and neurodegenerative diseases, such as Alzheimer’s, could be treated by targeting the immune system.
This approach, alongside other biological endeavours, has the potential to advance our understanding of the pathology of this devastating condition and lead to more effective, lasting treatments.
• Jonathan Cavanagh is Professor of Psychiatry at the University of Glasgow