Revisiting old ideas and assumptions, without clinical data, seems to be as good a start as any for puzzled scientists when it comes to the subject of depression, anxiety, and seasonal affective disorder (SAD). Categorizing these medical conditions into addictions or disorders has also not helped in discovery and treatment. This is not to say that behavioral counseling and certain selective serotonin re-uptake inhibitors known as SSRI, better known as anti-depressant drugs, do not help a percentage of the population. However, these methods are purely based on trial and error.
Over the past 15 years, there have been advances made by researchers in making more than just an effort in understanding the complexity of the brain and pinpointing areas of chemical balances.
In the 1950s, it was discovered that the Nucleus Accumbens (NAc) was associated with the ability to feel pleasure. Robert C. Malenka, M.D., Ph.D., Pritzker Professor of Psychiatry and Behavioral Sciences at Stanford University School of Medicine, decided to take a closer look at this pleasure circuit since it seemed to be lacking in many diagnosed with depression. What he and his colleagues discovered was that it was not as much the specific region of the brain as much as the circuit activity that crossed through many complex regions.
Dr. Malenka has become a leading expert on the tiny gaps, called synapses, that occur during the transmission of nerve cell activity signals. The challenge is great, since there are trillions of synapses in the human brain. Recently, melanocortin circuit’s contribution to anhedonia-like behavior was found, and Dr. Malenka has high hopes in identifying a potentially new pathway of intervention in depression. Melanocortin is a hormone that affects appetite in humans and further, turns off the brain’s ability to experience pleasure when an animal is stressed.
Monoamine oxidase loss is the basis of another study investigated by Dr. Jeffrey Meyer, Tier 1 Canada Research Chair in Neurochemistry of Major Depression at the Centre for Addiction and Mental Health in Toronto, Ontario. Monoamine oxidase (MAO-A) is an enzyme that breaks down chemicals like serotonin, norepinephrine, and dopamine.
Dr. Meyer discovered that there was a huge increase in MAO-A in patients with major depression diagnosis. Knowing that this was a significant breakthrough in tracking monoamine transporters, his team created a model to follow, like a road map. This will take the guess work out of watching how chemicals, like serotonin and dopamine, increase or decrease at different rates based upon transporter density. Researchers are now moving on to the next step in why MAO-A levels are raised in the brain and how to prevent it.
Dr. Marina Picciotto, Ph.D., Professor of Neurobiology and Pharmacology at Yale University, and a team of researchers, have proven a biological cause for depression and anxiety, one which was previously dismissed in theory. Acetylcholine is a neurotransmitter that was overshadowed by a signal-carrying chemical, called serotonin, as a leading cause of depression. While serotonin is important in the scheme of transmission, it is not nearly as powerful as acetylcholine.
An enzyme called acetylcholinesterase (AChE) has been found to lower acetylcholine levels. The team discovered while studying mice that were treated with Prozac, that the AChE levels raised considerably, and even higher levels of acetylcholine were noted. This once questionable area of treatment became understandable, and showed why SSRI anti-depressants were valuable in alleviating depression.
The relationship between serotonin and acetylcholine signaling systems has not yet become clear, but by finding the cause of depression, treatments can now be studied from a different point of view.
Genes and Chemicals
It has already been discovered that certain genes make individuals more susceptible to low moods and how their treatment with anti-depressant drugs may differ from the next person. However, by majoring this hurdle, scientists can now focus on how specific regions of the brain changes in individuals.
For example, the hippocampus is smaller in some depressed people. Scientists’ hypothesis lies in the fact that new nerve cells have to be grown in order to combat the deteriorating cells that cause depression. In animals, it was found that the use of anti-depressants spurred the growth and enhanced branching of nerve cells in the hippo-campus.
New neurons, a process called neurogenesis, that are stimulated by drugs specifically designed for strengthening nerve cell connections and improving the exchange of information between nerve circuits, could be the answer in treating depression. Scientists have pinpointed several types of neurotransmitters; these include Acetylcholine, Serotonin, Norepinephrine, Dopamine, Glutamate, and Gamma-aminobutyric acid (GABA). By studying each one of these transmitters and creating new chemicals that enhance their existence, depression, anxiety, and SAD could easily be treated.
It seems that researchers are onto something; something that can aid in treatment soon, others years down the road. While every one of these discoveries, including herbal remedies, seem deserving of further testing, let us not forget that the brain is a very complex machine, and that it may take a collaboration of findings in order to reach an answer for different individuals.
Featured photo credit: Gratisography via pexels.com
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