User:Choi.kel/sandbox

Article Evaluation

I evaluated the Public education and outreach article on the Neuroscience Wikipedia page. This article remains neutral and does not attempt to persuade readers on a certain stance. All of the major facts had citations attached to them; I checked a few citation links and the ones that I checked did work. This article's talk page mostly seemed to consist of editors attempting to better the article and bring it to "Good Article" status. This article is rated as B-class and is a part of a few WikiProjects: WikiProject Neuroscience, WikiProject Biology, WikiProject Philosophy, WikiProject Science, and WikiProject Education.

Unit Two Article Project

Potential articles and ideas on how to improve:

1. 5-HTTLPR (can click wikilink for article): add research suggesting that the 5-HTTLPR is associated with sleeping problems and insomnia
2. Insomnia (can click wikilink for article): introduce 5-HTTLPR genotype and how it is potentially related to insomnia

Final project article:

For my article project, I would like to contribute to the 5-HTTLPR article on Wikipedia. I have found research supporting the notion that the 5-HTTLPR gene is associated with insomnia, but it is not mentioned in the 5-HTTLPR article on Wikipedia. I plan on adding research regarding the gene's association with both sleep quality and insomnia. I also found a source that argues the gene NOT being associated with symptoms of depression, which I would like to add to the "neuropsychiatric disorders" section.

Proposed Bibliography

1. Brummet, Beverly, et al. “Sleep Quality Varies as a Function of 5-HTTLPR Genotype and Stress.” Psychosom Med, vol. 69, no. 7, 2007, pp. 621-624. 
2. Serretti, A, et all. “Serotonin transporter gene (5-HTTLPR) is not associated with depressive symptomatology in mood disorders.” Molecular Psychiatry, vol. 4, 1999, pp. 280-283.
3. Deuschle, Michael, et all. “Association between a Serotonin Transporter Length Polymorphism and Primary Insomnia.” Sleep, vol. 33, no. 3, 2010, pp. 343-347.

WIKI ARTICLE DRAFT (Improving 5-HTTLPR)

Existing section:

Alleles[edit | edit source]

The serotonin transporter gene (SLC6A4) with the 5-HTTLPR is located on chromosome 17.

The polymorphism occurs in the promoter region of the gene. Researchers commonly report it with two variations in humans: A short ("s") and a long ("l"), but it can be subdivided further. In connection with the region are two single nucleotide polymorphisms (SNP): rs25531 and rs25532.

One study published in 2000 found 14 allelic variants (14-A, 14-B, 14-C, 14-D, 15, 16-A, 16-B, 16-C, 16-D, 16-E, 16-F, 19, 20 and 22) in a group of around 200 Japanese and Caucasian people. The difference between 16-A and 16-D is the rs25531 SNP. It is also the difference between 14-A and 14-D.

Some studies have found that long allele results in higher serotonin transporter mRNA transcription in human cell lines. The higher level may be due to the A-allele of rs25531, such that subjects with the long-rs25531(A) allelic combination (sometimes written L_A) have higher levels while long-rs25531(G) carriers have levels more similar to short-allele carriers. Newer studies examining the effects of genotype may compare the L_A/L_A genotype against all other genotypes. The allele frequency of this polymorphism seems to vary considerably across populations, with a higher frequency of the long allele in Europe and lower frequency in Asia. Despite speculation to the contrary, the population variation in the allele frequency is more likely due to neutral evolutionary processes than natural selection.

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** Adding after "The polymorphism occurs in the promoter region of the gene. Researchers commonly report it with two variations in humans: A short ("s") and a long ("l"), but it can be subdivided further." --> The short (s)- and long (l)- alleles have been thought to be related to stress and psychiatric disorders³.

** adding section on the amygdala

Amygdala

The 5-HTTLPR has been thought to predispose individuals to affective disorders such as anxiety and depression. There have been some studies that test whether this association is due to the 5-HTTLPR's effects on the reactivity of the human amygdala. In order to test this, researchers gathered a group of subjects and administered a harm avoidance (HA) subset of the Tridimensional Personality Questionnaire as an initial mood and personality assessment ⁴. Subjects also had their DNA isolated and analyzed in order to be genotyped. Next, the amygdala was then engaged by having the subject match fearful facial expressions during an fMRI scan (by the 3-T GE Signa scanner). The results of the study showed that there was bilateral activity in the amygdala for every subject when processing the fearful images. However, the activity in the right amygdala was much higher for subjects with the s-allele, which shows that the 5-HTTLPR has an effect on amygdala activity. Meanwhile, there did not seem to be the same effect on the left amygdala.

* I will be inserting a section on insomnia:

Insomnia

There has been speculation that the 5-HTTLPR gene is associated with insomnia and sleep quality. Primary insomnia is one of the most common sleep disorders and is defined as having trouble falling or staying asleep, enough to cause distress in one's life. Serotonin (5-HT) has been associated with the regulation of sleep for a very long time now ³. The 5-HT transporter (5-HTT) is the main regulator of serotonin and serotonergic energy and is therefore targeted by many antidepressants³. There also have been several family and twin studies that suggest that insomnia is heavily genetically influenced. Many of these studies have found that there is a genetic and environment dual-factor that influences insomnia. It has been hypothesized that the 5-HTTLPR genotype is related to poor sleep quality and, therefore, also primary insomnia. It is important to note that research studies have found that the 5-HTTLPR does not cause insomnia, but rather may predispose an individual to experience worse quality of sleep when faced with a stressful life event.

Brummet

The effect that the 5-HTTLPR gene had on sleep quality was tested by Brummet in a study conducted at Duke University Medical Center from 2001-2004. The sleep quality of 344 participants was measured using The Pittsburgh Sleep Quality Index. The study found that caregivers with the homozygous s-allele had poorer sleep quality, which shows that the stress of caregiving combined with the allele gave way to worse sleep quality. Although the study found that the 5-HTTLPR genotype did not directly affect sleep quality, the 5-HTTLPR polymorphism's effect on sleep quality was magnified by one's environmental stress¹. It supports the notion that the 5-HTTLPR s-allele is what leads to hyperarousal when exposed to stress; hyperarousability is commonly associated with insomnia.

Deuschle

However, in a 2007 study conducted by a sleep laboratory in Germany, it was found that the 5-HTTLPR gene did have a strong association with both insomnia and depression both in participants with and without lifetime affective disorders. This study included 157 insomnia patients and a control group of 836 individuals that had no psychiatric disorders. The subjects were then genotyped through polymerase chain reaction (PCR) techniques. The researchers found that the s-allele was greater represented in the vast majority of patients with insomnia compared to those who had no disorder³. This shows that there is an association between the 5-HTTPLR genotype and primary insomnia. However, it is important to consider the fact that there was a very limited number of subjects with insomnia tested in this study.

References

1. Brummet, Beverly, et al. “Sleep Quality Varies as a Function of 5-HTTLPR Genotype and Stress.” Psychosom Med, vol. 69, no. 7, 2007, pp. 621-624.
2. Serretti, A, et all. “Serotonin transporter gene (5-HTTLPR) is not associated with depressive symptomatology in mood disorders.” Molecular Psychiatry, vol. 4, 1999, pp. 280-283.
3. Deuschle, Michael, et all. “Association between a Serotonin Transporter Length Polymorphism and Primary Insomnia.” Sleep, vol. 33, no. 3, 2010, pp. 343-347.