Researchers from the University of Toronto and the University College London are reporting a new imaging technique that could reveal the brain mechanisms of depression, anxiety and other mood disorders, as well as reveal genetic predispositions.
The technique, dubbed neural neuroimaging, could lead to new treatments for depression, which has been linked to an increased risk of other mental health disorders.
It could also help clinicians develop treatments that target other psychiatric disorders.
The researchers’ work was published this week in the journal PLOS One.
Neuroimaging is a technique to take a snapshot of a person’s brain using brain scanning.
The process uses a computer-generated image of a subject’s brain to generate a 3D image of their brain tissue.
This image then is used to determine how well a person responds to a specific stressor or mental stressor.
The image also helps to identify whether or not someone is susceptible to developing mental illnesses, such as anxiety or depression.
The team used a brain scan to examine how the brain processes a stressor in mice.
The study found that a particular gene, called SLC12A4, is involved in regulating the release of a hormone called corticosterone, which is involved with stress responses in the brain.
This hormone has been implicated in depression and anxiety, and is known to be altered in people with these disorders.
They found that SLC4A1 was also downregulated in mice with depression and the researchers also found that the gene was downregulated more in mice that were genetically predisposed to developing anxiety.
They also found evidence of a gene that has been associated with depression in humans, called P300, in the brains of people with depression.
“The researchers found that, in mice, SLC1A4 and P300 were downregulated together, meaning that the P300 gene had an impact on the regulation of corticosteroids and other stress-related hormones in the nervous system,” said co-author David Haggerty, a professor in the department of physiology at the University at Buffalo.
“This suggests that P300 is involved not only in regulating stress-induced cortisol levels in the central nervous system but also in the regulation and modulation of neuroinflammation in the hippocampus.”
In the mouse model, the team found that when the mice were placed under stress, the SLC14A2 gene, which codes for an enzyme that breaks down cortisol, was down regulated.
They then showed that the mice with depressed or anxious genes also had decreased levels of SLC18A1, an enzyme responsible for making cortisol.
They were also able to show that SSC1A2, which encodes a protein involved in the production of cortisol, also was down-regulated in the mice that had depressed or anxiety genes.
The findings suggest that SCC4A, which also encodes an enzyme involved in cortisol production, was also altered in the depressed mice, HaggerTY said.
“Our findings suggest a link between depression and SLC16A1 and SSC2A2,” Hagger.
The SLC2A1 gene was also upregulated in depressed mice.
“We also found the SSC6A1 protein was upregulated, which may be related to the decrease in the expression of the cortisol transporter, which leads to increased cortisol release in the cortex,” Hagan said.
Haggert said that these findings suggest SLC6A2 may play a role in depression.
Other studies have also found a link in mice to a loss of the S-protein, which occurs when the S6A3 gene is downregulated.
However, the authors said that the results of their study do not indicate whether this gene is a cause of depression or if it is an important gene that regulates other genes involved in depression in people.
They said that they hope to further investigate whether SLC-6A is involved as a potential target for new treatment options for depression.
Hagan added that the findings could also be useful for people with other psychiatric illnesses.
“There are a number of gene variants that have been associated in people who have other mental illnesses such as bipolar disorder, schizophrenia, depression, autism, anxiety or other neuropsychiatric disorders,” Hagg.
“One of the ways to identify genes that are associated with a person has to do with the degree of their depression,” he said.
The results of the study were also published in the Proceedings of the National Academy of Sciences.
The research was funded by the National Institutes of Health.