Major depressive disorder is a highly familial illness and the leading cause of disability worldwide for persons 15 to 44 years of age. It is associated with increased mortality resulting from cardiovascular disorder, poor personal care, and suicide. Genetic and environmental factors and their interactions are important in its pathogenesis, however, the abnormalities of brain structure and function that mediate these effects have not yet been identified.
Now, a study from researchers at Children’s Hospital Los Angeles and Columbia University shows a link between a particular allele for serotonin found at a higher frequency in those at risk of depression because of family history, and those who go on to develop major depressive disorder. The team state that their findings, building on a 30-year, three-generation study of depressed individuals, provides a better understanding of the familial risk for depression and the role neuroplasticity might have in increasing the risk of developing depression. The study is published in the journal Psychiatry Research: Neuroimaging.
Previous studies show that several genes have been associated with depression, especially those genes that alter serotonin signaling. Serotonin is a chemical messenger in the brain that acts as a mood stabilizer. Earlier studies from the lab showed that individuals at familial risk for depression, whether or not they have exhibited signs of depression in the past, have a pattern of thinning in certain cortical regions of the brain. Data showed that additional brain loss occurred in other areas of the brain in those who did manifest depressive symptoms. A genetic variation, or allele, found in the promoter region of the serotonin transporter was found to affect this brain loss. The current study assessed whether the effects of familial risk were specifically modulated by this serotonin-transporter-linked polymorphic region (5-HTTLPR).
The current study utilised brain MRI images of 120 individuals, those at both high and low familial risk of depression, along with genotype data. Results show that among those at low risk for depression, the ‘S’ (short) 5-HTTLPR allele is associated with a thinner cortex than those with the ‘L’ (long) 5-HTTLPR allele.
Data findings show that in the individuals at high risk for depression because of their family history, the correlation is actually reversed and more cortical thinning is found in those with the ‘L’ allele. In addition, the group observed that those with the ‘S’ allele were at higher risk of developing depression than those with the ‘L’ allele when exposed to the same type and amount of stressors. Therefore, the lab hypothesize that brain plasticity also plays a role in depression.
The team surmise that their data suggests that those with the ‘L’ allele or genetic variation can better adapt to their environment. They go on to add that those with the ‘S’ allele appear to have lower brain plasticity and perhaps have fewer compensatory factors in the brain that allow them to adapt to adverse conditions. For the future, the researchers state that further scientific studies looking at cortical thickness, combined with genotyping, could also have the potential to predict who will develop depression and how individuals respond to anti-depressant medications.
Source: Children’s Hospital Los Angeles
biomarker, depression, environmental factor, epigenetics, genetics, healthinnovations, marker, neuroanatomy, neurobiology, neurogenetics, neuroimaging, neuroinnovations, neuroplasticity, Serotonin system
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