LSD Causes Schizophrenia???

Schizophrenia is a mental disorder that is classified by its symptoms of abnormal social behavior and the inability to discern what is real from what is not. Many symptoms are circled around having false beliefs, unclear thinking, hearing voices, and reduced social engagement. If you know anyone with schizophrenia you know that this disorder can have a detrimental effect on the individual's life. With that said, no one really knows the absolute causes of this disease. It is believed that environmental factors along with brain chemistry and genetics play a huge role in the progression of the disorder. In research regarding this topic, scientists have discovered that aromatic l-amino acid decarboxylase (AADC) concentrations in blood serum is increased. AADC is the rate limiting step in the production of 2-phenylethylamine (2PE), which is a known psychotogenic (causes the individual to experience psychosis) and dopamine agonist. This is particularly useful knowledge because it is also known that schizophrenia is a highly dopaminergic system. 

To play off the knowledge of the knowns about schizophrenia, scientists at the University of Wales College of Medicine, tested to see what two psychotogenic drugs, LSD and PCP, do to the levels of AADC  mRNA levels in rats. LSD and PCP are two known hallucinogenic drugs but they are considered non-dopaminergic, as LSD affects serotonin levels and PCP affect many neurotransmitters but mainly glutamate. The reason why these two drugs were chosen is because they are used as schizophrenia models in animals but they both have different structures and different pharmacologies.

In this study, however, it was shown that both LCD and PCP have small effects on AADC gene expression, with LCD acting as a probe for exon 8. The mechanism of the up-regulation of AADC mRNA is unclear for both of these drugs but the mRNA change patterns for both of the drugs is really similar. This study does further prove that using these drugs could cause the expression of the gene that codes for AADC and in turn produces 2PE, but the evidence in this study was not statistically significant. In humans there are two alternative exons at the 5' non-coding region of the gene one being predominate and lacks exon 3 causing it to be short 38 amino acids and does not catalyse the conversion of DOPA into dopamine. This shorter form could be the cause of phenylalanine converting to 2PE. Since rats do not experience schizophrenia then this primary version of the gene might not exist or exist in such small quantities that caused the statistical insignificance. There might have to be other types of studies that would have to be tested on individuals that actually use these drugs or other animals that experience schizophrenia to get statistically important results.