Identifying the gene-brain mechanisms that contribute to anxiety


There are a number of anxiety disorders

  • Generalised Anxiety is not specific to one particular thing but can be about anything and everything.
  • Social anxiety disorder occurs in public situations where there is perceived risk of being judged or laughed at by others.
  • A panic attack involves sudden overwhelming feelings of uneasiness, fear or terror. A person may feel they are about to have a heart attack or die. Panic disorders are diagnosed when this happens repeatedly, or when a person fears future panic attacks.
  • Agoraphobia is anxiety about being in situations from which escape might be difficult or embarrassing if you have a panic attack.
  • Specific phobias usually involve intense and ongoing fear of particular objects or situations such as bridges or dogs.
  • Obsessive compulsive disorder (OCD) occurs when particular, sometimes repetitive, compulsive acts must be enacted in order to calm an anxiety, such as checking things numerous times.
  • Post-traumatic stress disorder (PTSD) is often triggered by a major traumatic event, such as being assaulted or in an accident. It involves upsetting memories, flashbacks, nightmares, and difficulties sleeping.

Anxiety disorders can be caused by genetic influence, poor physical health, stress or a thinking style that involves anticipating the worst and negative self-talk. Cognitive Behavioural Therapy has been found to be an effective way to alter unhelpful thoughts and behaviours that can contribute to anxiety.

Our research

Our research focuses on identifying the gene-brain mechanisms that contribute to increased severity of anxiety and depression symptoms. We evaluate various measures of brain function including neurocognitive performance tests, measures of magnetic resonance imaging scan (MRI), autonomic function and electrophysiological (EEG) function at rest and during cognitive tasks.

A lot of our previous work focused on identifying such mechanisms from participants drawn from the normal population. We are also focusing on understanding the same mechanisms but in a large cohort of Australian adult twins – both identical and non-identical twins – who have been tested over time. The added value of a twin design is that we are able to define the percentage contribution of genetics and environment for each measure, which helps pinpoint the measures to focus on when trying to identify specific genes or life experiences that are important in shaping our brain development.

The aim of this work is to understand what predicts anxiety and depression, the optimal ways to prevent it with intervention, as well as potential predictors of treatment response.

What we have discovered

Using the normal population data, the Gatt and Schofield Groups have shown the differential impact of childhood trauma on brain volume and brain function using measures such as EEG, MRI and autonomic activity. We have shown, for instance, that exposure to early life trauma has a detrimental impact on brain volume and/or function that is exacerbated when combined with specific genetic variants such as the BDNF, HTR3A, and 5-HTT-LPR genes. We have also shown the type of trauma exposure (interpersonal versus non-interpersonal trauma, and child versus adult trauma) has a varying impact on depression and anxiety symptoms.

In our twin cohort data, the Gatt Group has also started to show the levels of heritability of anxiety and depression symptoms, and how shared genetic and environmental mechanisms largely contribute to both anxiety and depression symptoms (Burton et al., 2015). In these studies, we are focusing in particular on variation between males and females give known sex differences in prevalence of these disorders. Our findings are starting to show why men and women may differ in prevalence and the potential mechanisms this may impact, including neural responses to specific emotions (e.g., happy versus sad emotions).

Current projects

Our current projects include a focus on the impact of normal variation in anxiety and depression symptoms in the general population, as well as the impact of symptoms and their treatment in clinical groups (e.g., PTSD and Major Depression).

Project 1 – In our large adult cohort of 1,600 twins, we are identifying the factors that contribute to symptoms of anxiety and depression and potentially clinical disorder over time. This includes a focus on mechanisms such as genes, environment (e.g., life experiences, parenting styles), measures of cognitive function, EEG and neuroimaging.

Project 2 – We are also involved in some collaborative work with other groups focusing on identifying neural mechanisms such heart rate variability and EEG brain function in clinical disorders such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD).

See what’s going on at NeuRA