Depression is more than just tearfulness or feelings of sadness. It refers to a range of mood and other symptoms that are intense, long-lasting and distressing to the person. These symptoms will likely interfere with a person’s day-to-day life and relationships.
The causes of depression can vary from person to person. For some, stressful life events such as the loss of a relationship or job, long-term unemployment, physical health issues, family problems, or the death of a loved one might trigger depression. For others, there is no obvious cause.
The offspring of individuals with bipolar disorder are at increased risk of mental illness, but our tools to predict which of these genetically at-risk young people will eventually develop disorder are very imprecise. Longitudinal studies that ascertain at-risk participants and monitor them prospectively are an effective approach for identifying early clinical and biological markers of future illness. In collaboration with the Black Dog Institute plus groups from four independent US-based sites, including: Johns Hopkins University; University of Michigan; Washington University in St. Louis; Indiana University; we are following a cohort of young kids and siblings of bipolar disorder patients with annual clinical, neurocognitive and lifestyle assessments; plus bi-annual brain imaging of the Australian participants. We are assessing the genetic load of multiple risk variants across the genome in these at-risk individuals to determine if we can use genetic information to help predict which individuals will ultimately transition to illness, and whether genetic load will influence early structural brain changes which are seen prior to onset of symptoms which lead to a clinical diagnosis.
We are also examining whether epigenetic changes – which occur on-top-of the DNA sequence in response to environmental influences – are involved in transition from health to illness. Early identification of those most likely to develop illness will provide a firm basis on which to develop preventive and early intervention strategies to reduce the impact of this devastating disorder.
In a collaborative study with Professors Kay Wilhelm and Phil Mitchell from the UNSW School of Psychiatry, Professor Peter Schofield and his team examined the genetic variation in the transporter protein that is involved in the reuptake of the neurotransmitter serotonin. There is an association between low serotonin transporter levels, stress and depression. The group has further shown that there is an association between the serotonin transporter genotypes and the way an individual copes with stress. This has led to further clinical studies correlating how individuals can use different methods to handle stress. Their research has significant implications for reducing the likelihood of developing depression and a planned future study will be to evaluate whether specific training in stress management, matched to an individual’s genotype, may lead to a reduction in the incidence of depression.
Originally Published by the Seattle Children’s Research Institute A study conducted by an international research team, which included investigators from NeuRA and the Seattle Children’s Research Institute, implicates variants in four genes as a primary cause of non-syndromic cleft lip and palate in humans. The genes, associated for the first time with cleft lip and palate, encode proteins that […]