This video discusses the current standard of care for treating depression, which is based on the monoamine deficiency hypothesis. This hypothesis assumes that one of three neurotransmitters in the brain is deficient, causing depression. However, with over a hundred neurotransmitters and billions of connections in the brain, this hypothesis is limited. Researchers have found that neurotransmitters like glutamate and GABA may play a role in depression. Chronic stress can lead to a loss of synaptic connections in the brain, contributing to the biology of depression. Understanding the neurobiology of depression can help develop targeted treatments for the disease. This marks a paradigm shift in psychiatry.
Key Insights:
- The current standard of care for depression is based on the monoamine deficiency hypothesis.
- There are over a hundred neurotransmitters in the brain and billions of connections between neurons, limiting the monoamine deficiency hypothesis.
- Abnormalities in neurotransmitters like serotonin and norepinephrine cannot fully account for the symptoms of depression.
- Glutamate and GABA, neurotransmitters involved in regulating mood and emotion, are potential alternative causes of depression symptoms.
- Severe and chronic stress can lead to the loss of synaptic connections in circuits that regulate mood, contributing to the biology of depression.
- Understanding the neurobiology of depression helps develop targeted treatments.
- Treating depression effectively can restore the brain to a healthier state.
- Depression is often a long-term disorder, necessitating new and more effective treatment approaches.
- We are now in an era of psychiatry that considers the brain as a complex neurochemical organ rather than solely focusing on monoamine deficiencies.
Transcript
The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially presuming that one of three neurotransmitters in the brain is deficient or underactive. Neurotransmitters can be thought of as the chemical messengers within the brain. It’s what helps one cell in the brain communicate with another to pass that message along.
But the reality is there are more than a hundred neurotransmitters in the brain and billions of connections between neurons. So we know that that’s a limited hypothesis. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine.
However, norepinephrine and serotonin did not seem to be able to account for the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain involved in regulating mood and emotion, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. We know that these two, which are the most ubiquitous and abundant neurotransmitters in the brain, actually regulate how the brain is changing over time and adapting.
When you are exposed to severe and chronic stress like people experience when they have depression, you lose some of these connections between the nerve cells and the communication in these circuits becomes inefficient and noisy. Because of the noisy communication in the circuits involved in regulating mood and emotion, we think that the loss of these synaptic connections contributes to the biology of depression.
It’s critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses and we can start to target treatments based on that. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is when you treat that depression effectively, the brain goes back to looking like a healthy brain.
We recognize that the treatment for depression is a long-term process because for many people depression is a long-term disorder. So we need new treatments. We’ve needed new ways to approach depression for people that haven’t responded well to their prior treatments. We are in a new era of psychiatry. This is a paradigm shift away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ.
