Major Depressive Disorder and chronic stress are both characterized by atrophy of neurons and loss of synapses (centers of neurotransmission that deliver neural impulses) in specific brain areas. It’s been recently shown that the prefrontal cortex of subjects with Major Depressive Disorder, analyzed postmortem, contains abnormally low expression levels of a protein called mTORC1, which controls protein synthesis during cell growth and synapses remodeling.
In line with this, it was also observed that in rats some antidepressants augment mTORC1 levels, and this is associated with increased synapses formation in the prefrontal cortex. But what controls mTORC1 expression in the brain? And more importantly, would it be possible to manipulate mTORC1 levels therapeutically to rescue neuronal function?
Stress and TORC1
In a study just published in Nature Medicine, Ota and colleagues from Yale University have identified a new mechanism that is at least in part responsible for the brain alterations caused by loss of mTORC1. The scientists focused on a gene called REDD1 whose product is known to inhibit mTORC1 function. They found that in individuals that were affected by Major Depressive Disorder, high levels of REDD1 correlated with low mTORC1 expression, suggesting a possible link between these two molecules.
In line with this, it was also observed that in rats some antidepressants augment mTORC1 levels, and this is associated with increased synapses formation in the prefrontal cortex. But what controls mTORC1 expression in the brain? And more importantly, would it be possible to manipulate mTORC1 levels therapeutically to rescue neuronal function?
Stress and TORC1
In a study just published in Nature Medicine, Ota and colleagues from Yale University have identified a new mechanism that is at least in part responsible for the brain alterations caused by loss of mTORC1. The scientists focused on a gene called REDD1 whose product is known to inhibit mTORC1 function. They found that in individuals that were affected by Major Depressive Disorder, high levels of REDD1 correlated with low mTORC1 expression, suggesting a possible link between these two molecules.
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