HOW DEPRESSION AFFECTS THE BRAIN

The current treatment for depression is based on the monoamine deficiency hypothesis. This hypothesizes that one of three neurotransmitters in the brain is deficient or underactive. Neurotransmitters can be thought of as the chemical messengers within the brain. They help one cell in the brain communicate with another to pass a message along. But this hypothesis is limited because there are more than a hundred neurotransmitters in the brain and billions of connections between neurons. So we know that it's not just one abnormality that's causing depression, it could be dozens of different factors. For decades, we thought that the primary cause of depression was an abnormality in these neuro-transmitters specifically serotonin or norepinephrine. However, serotonin and norepinephrine couldn't account for all of the symptoms of depression in people who had major depression. Instead, glutamate and GABA, which are two of the most ubiquitous and abundant neurotransmitters in the brain, were potential causes for their symptoms. We now know that these two chemicals regulate how the brain is changing over time and how it adapts.

Stress causes the communication between nerve cells to break down,, leading to depression. In comparison to a healthy brain, a depressed brain has lost these connections and communication is inefficient and noisy. Because of this, it is important to understand the neurobiology of depression so that we can start to target treatments based on that. There are clear differences between a healthy brain and a depressed brain, and when you treat depression effectively, the brain goes back to looking like a healthy one. We recognize that the treatment for depression is a long-term process because for many people this is a long-term disorder. So we need new treatments that will work better for people who haven't responded well to their past treatments. This is an era of psychiatry where we're starting to shift away from models that focus on monoaminergic deficiency. How long-term are the changes?

Major depressive illness (clinical depression) has long-term repercussions on the brain, but it is unclear exactly what those effects will be or how long they will last. These questions are still being researched. Research, however, indicates that the impacts might persist.

Any degree of clinical depression may have an adverse effect on the brain, but persistent or recurrent depression may have a particularly harmful effect. The effects of depression on the brain may accumulate over time, according to some research, and some of these alterations (such as those to the hippocampus in patients with lifelong major depressive disorder) may still exist years after a depressive episode. Translocator protein concentrations also rise in depressed individuals. These chemicals in the brain have been linked to inflammation in the brain, and research indicates they can:

harm or destroy brain cells

Stop them from growing more

interfere with thinking and hasten the ageing of the brain

Even if levels recover to normal, transient spikes in ageing and reduced new growth can still have long-lasting effects. One thing is certain: persistent depression most likely does alter our brains significantly and permanently. Depression's neurobiology is quite complex. Depression often results from an inability to handle stress. A significant factor in this is an overactive amygdala that is (mis)regulated by the prefrontal cortex. Furthermore, an overactive amygdala may lead to a cognitive bias that favours a negative perception of both the outside world and oneself. Adding insult to injury, the decline in the rewarding effects of dopamine in the nucleus accumbens (NAc) appears to coincide with the rise in unpleasant thoughts and emotions, suggesting that these two phenomena are related. These biological findings are in line with behavioral findings that depressed individuals exhibit a negative cognitive bias and anhedonia.