Anxiety Can Disrupt Mitochondrial Function
Anxiety is a serious mental disorder characterized by panic attacks and a strong emotional response to stress. It can be initiated by stressful life events, such as bereavement, divorce and conflict.
It is known that some people are more susceptible to anxiety than others, as not all who experience stressful life events necessarily experience anxiety. It is thought that this disparity could lie in genetic factors that can pre-dispose people to experience anxiety symptoms. A new study aims to investigate the biological pathways that underpin responses to stress.
Two genetically different strains of mice were used in the study, B6 and D2. D2 mice are known to be genetically susceptible to stress, whilst B6 are more stress resistant.
A male mouse was introduced to the territory of another male mouse of the same strain for 10 days, to initiate conflict between them and a stressful situation for the non-dominant mouse. All the defeated mice experienced stress, but not all developed symptoms of anxiety, defined in mice as socially isolating themselves. 89% of the D2 mice and 30% of the B6 mice displayed social avoidance behaviours, demonstrating that genetic disposition plays a strong role in the development of anxiety symptoms.
However, the stress susceptible mice of both strains displayed distinct gene expression patterns not shared by the stress resistant mice of their respective strains. The differences in expression were shown to affect the metabolic pathways in the brain mitochondria, the energy powerhouse of the cells. The disrupted pathways included energy processing and hormone signalling.
Patients with anxiety had their blood tested after experiencing a panic attack. It was found that they also experienced changes in their mitochondrial pathways, suggesting that anxiety affects the body’s energy processing capabilities.
It is difficult to develop effective drugs for mental disorders, as the biological mechanisms that underpin these conditions are poorly understood. Recognising that anxiety disrupts mitochondrial pathways could provide a new therapeutic avenue for drug development.