Jun 16, 2017 11:17 AM EDT
Early Life Stress Encodes Specific Brain Regions That Trigger Depression [VIDEO]
A recent study revealed that inherited genes have nothing to do with the risk of depression later in life. Rather, it when a person experiences early-life stress affecting how the brain functions and responds to challenges and adversity.
A team of researchers from Icahn School of Medicine at Mount Sinai studied the role of genetics in depression. They discovered that the inherited genes are not the culprit but the molecules that regulate these genes.
These molecules affect how the genes function when the person experiences early life stress. Catherine Peña, the lead investigator of the study, said that the mice that experienced disruptive maternal care when they were young had changes in their genes which placed them in a depression-like state. This occurred even before they showed symptoms of depression.
These molecules include specialized proteins that encode long-lasting transcription programming in the specific reward region of the brain. One particular protein that caught the attention of the researchers was the orthodenticle homeobox 2, which serves as the master regulator of these genes.
Young mice that experienced stress during a sensitive period of their development showed suppressed Otx2 in the ventral tegmental area or VTA of the brain. However, these suppressed Otx2 has already created alterations in the genes that last through adulthood.
The mice that experienced early life stress appeared and behaved normally until they experience another stress during their adulthood. Once this happens, these mice begin to exhibit depression.
The study confirms what other researchers have been speculating regarding the connection between the relationship of early life stress experiences and depression. It has provided concrete evidence based on genetics how adult depression develops.
It also gave insight to doctors in providing the right treatment methods to patients experiencing depression.
The study was published in the journal Science.
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