According to University of British Columbia Professor Rebecca Todd, the gene ADRA2b, if deleted, results in an amplification of an individual's profundity in emotional recall. This causes individuals to experience the negative side of situations more profoundly. Professor Todd concentrated on human trials with 200 participants whom she asked to analyze the positive, neutral, and negative words that they were presented. All participants equally recalled positive words whereas the individuals with the ADRA2b mutation were more likely to remember the negative words than the individuals without the mutation.
Because we cannot observe the internal mechanisms of a human brain without encrouching on strong ethical boundaries or facing large expenses operating machinery, we are able to observe and deduce the results by engineering animals that have analogous mutations.
An entire group of mice may be bred to exhibit the mutation similar to the deletion of ADRA2b in humans. From there, an entire slew of research opportunities appear. The animal's brain may be studied, upon death, in thin, lateral slices beneath a microscope after careful preservation to determine whether the lack of ADRA2b analogue influenced the brain structure of the affected mouse as compared to a wild type mouse (a mouse that exhibits the common genetic frequency that occurs naturally). These regions of the brain may be more closely observed in terms of protein composition while mice with the same mutation are still alive. I will discuss this in the next paragraph. The corresponding parts of the brain in a human can be studied through imaging systems so that future reparative treatment can be applied directly to the deficient region after such technologies are refined enough to operate without adversely effecting unintended genes.
A microdialysis tube can be placed within the brain of a mouse to collect samples of proteins that are present in the region of the brain that would originally have been influenced by the ADRA2b gene. By analyzing the composition of the collected sample, scientists can deduce the role of ADRA2b proteins in inhibiting production of negative thought inducing proteins directly or indirectly (by increasing the production of another protein that blocks the production of negative thought inducing proteins). What we find with mice can be applied to humans through individuals that naturally lack genes that function alongside ADRA2b to observe which genes ADRA2b proteins are responsible for influencing. Such a process is difficult and expensive because non-invasive techniques must be used to preserve the ethical boundaries associated with use of human participants in a study (and I'm not even mentioning the effort it takes to locate individuals with these mutations).
Upon the completion of study through the use of genetically modified mice, we can apply what we learned about the deletion of the ADRA2b analogue from the mouse and how that influenced the structure and function of the brain and allocate funds to a human study such as the one that Professor Todd performed. Eventually, what we learn about the structures that ADRA2b influences and is influenced by will aid in developing a method to insert that gene into individuals that experience debilitating depression influenced by the deletion of ADRA2b. This, of course, would be the work of a science fiction writer but it's important to remember that genetic engineering in animals and plants was once considered the same way.
Bibliography:
Anthes, Emily. Frankenstein's Cat: Cuddling up to Biotech's Brave New Beasts. 1st. Edition. New York: Scientific American, 2013. Print.es, Emily
Ellison, Annie. "Glass always half-empty? Your genes may be to blame - British Columbia - CBC News." CBC.ca - Canadian News Sports Entertainment Kids Docs Radio TV. N.p., 11 Oct. 2013. Web. 11 Oct. 2013. <http://www.cbc.ca/news/canada/british-columbia/glass-always-half-empty-your-genes-may-be-to-blame-1.1959903?cmp=rss>.
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