User:JohannThomas2/Week4ProposedArticle

I have decided to focus a new topic as there was already a solid section of an article on my previous topic, epigenetics of childhood trauma. I plan on revising and improving the bit of information that wikipedia has on the epigenetics of bipolar disorder. Searching on wikipedia, I found that there is only a short little paragraph about the epigenetics of bipolar disorder in the article "Behavioral Epigenetics" and most of this information is since outdated. That section cites articles that are 10+ years old and contains what I perceive as conflicting information. I also checked the wiki page for Bipolar Disorder and while it was alluded to, there was no specific discussion of epigenetics. It only mentions that a combination of genetic and environmental factors can lead to bipolar disorder. The following review article, Epigenetic Drugs for Mood Disorders, (Jacob Peedicayil, Aniket Kumar, Epigenetic Drugs for Mood Disorders, Editor(s): Dennis R. Grayson, Progress in Molecular Biology and Translational Science, Academic Press, Volume 157, 2018, Pages 151-174, ISSN 1877-1173, ISBN 9780128135655, https://doi.org/10.1016/bs.pmbts.2018.01.005.) examines how epigenetics affect mood disorders and how current pharmacology treatments can be improved using potential epigenetic treatment.

For bipolar disorder specifically, the review article offers some useful insights that can be used to improve the information in the current section of the "Behavioral Epigenetics" wiki article.

Key points:

- It has been found in postmortem studies of patients with Bipolar Disorder that there is higher than expected activity for DNA methyltransferase-1 in the areas around the genes for Reelin and Glutamic Acid Decarboxylase-67 in the prefrontal cortex. Reelin is critical for development in the brain, so increased methylation of the genes for Reelin leads to reduced expression of the Reelin genes. Glutamic Acid Decarboxylase-67 is a vital enzyme for transforming glutamic acid into γ-amino butyric acid (GABA). In postmortem studies, patients with BD had lower expression of Glutamic Acid Decarboxylase-67 and Reelin.

- Upregulation of ten-eleven translocation 1 (TET1) was implicated in the review article as studies about the demethylation of DNA in patients with bipolar disorder.

- Promising preliminary studies showing the use of histone decacetylase (HDACi) to potentially aid treatment of bipolar disorder

- Hypermethylation of the promoter of the gene that encodes brain-derived neurotrophic factor has been found in patients with BD. This phenomenon has also been observed in patients with Major Depressive Disorder suggesting that this phenomenon potentially has a critical role to play in both bipolar disorder and major depressive disorder

- One study also found that in patients with bipolar disorder, modifications in the methylation of the promoter of the gene for the serotonin transporter, which is responsible for reputaking serotonin from the synaptic cleft back into the presynaptic neuron, was observed. Like how hypermethylation of the promoter of the gene that encodes brain-derived neurotrophic factor was found in patients with major depressive disorder, so was modifications in the methylation of the promoter of the gene for the serotonin transporter. This could also signal potential similarities in the disorders on a biochemical and epigenetic level and may provide insight into future treatments.

The review article contains a number of tables summarizing current research into the epigenetics of bipolar disorder and potential treatments for bipolar disorder along with current information about bipolar disorder and current treatments.