Depression and Genetics

After learning about loved ones who had suffered from mental illness, I was determined to learn more about this ‘invisible epidemic.’ I learned that today’s psychological treatments involve a lot of subjectivity and inconsistency when it comes to making diagnoses. Mood disorders such as depression and bipolar disorder have similar, overlapping symptoms to anxiety disorders and even learning disorders such as attention deficit hyperactivity disorder (ADHD). I chose to focus on three such disorders: depression, bipolar disorder and ADHD. The purpose of my research was to see if there is an underlying genetic difference between the three disorders that can be scanned for via Single Nucleotide Polymorphisms (SNPs) and from there, further explained. This has implications for genetic screening to create more accurate diagnoses, and advances mental disorder research by providing the exact pinpoint from which to develop treatments.

What is a Single Nucleotide Polymorphism (SNP)?
A SNP (pronounced ‘snip’) is a single base change in a single strand of DNA, resulting in a base pair change in a DNA double helix. The four nucleotide bases are Adenine, Cytosine, Guanine and Thymine, each with unique chemical properties. 6-carbon ringed pyrimidines include Cytosine and Thymine, and 2-ring fused purines include Adenine and Guanine. Together these bases are complementary, which means that pyrimidines pair with purines: C and G pair up, and A and T pair up in double-stranded DNA. If a base pair changes from the average genotype, genetic variations may occur.

What happens when someone has SNPs in their genetic code?
Most of the human population has some variation between genetic code—after all, that’s why we all look and behave differently! According to research from the NIH, humans have an average of 10 million SNPs in their DNA,one occurring every 300 nucleotides. SNPs occur most frequently in non-coding DNA regions (regionsbetween genes) and act as biological markers to help scientists locate genes associated with disease. When SNPs occur within genes or in regulatory regions, they can cause a more direct role in disease. If a SNP results in an amino acid different from the average human genome, protein structure may change. It is precisely a series of SNPs on vulnerable animo acids that leads to malformation of proteins, which makes it difficult for ribosomes to carry out the correct sequence, and for enzymes or drugs to bind to the protein. Researchers have found that SNPs may predict an individual’s risk of developing certain diseases or their response to drugs, the latter of which constitutes a field called pharmacogenomics which I hope to expand on.