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Article summary:
1. Genome-wide association studies have identified a large pool of genetic variants associated with schizophrenia, many of which are related to the glutamatergic signaling in the central nervous system.
2. This study used high-performance liquid chromatography (HPLC) and quantitative RT-PCR (qRT-PCR) to measure levels of glutamate and related amino acids, as well as mRNA and protein levels of pre- and post-synaptic key molecules in the post-mortem dorsolateral prefrontal cortex (DLPFC) and hippocampus of schizophrenia patients and non-psychiatric individuals.
3. Results showed significantly higher levels in l-Asn in both brain regions, while no alterations in other amino acids were detected.
Article analysis:
The article is generally reliable and trustworthy, providing evidence for its claims through the use of high performance liquid chromatography (HPLC), quantitative RT-PCR (qRT-PCR), western blotting analyses, and a hypothesis free Machine Learning analysis. The authors also provide detailed information on their methods, including sample size, demographic characteristics, confounders considered, statistical tests used, etc., which increases the trustworthiness of their results.
However, there are some potential biases that should be noted. First, the sample size is relatively small (20/brain region/clinical condition). Second, all subjects were deceased individuals; thus it is possible that some confounding factors may have been overlooked or underestimated due to lack of information about them prior to death. Third, although the authors did consider age and postmortem interval as confounders when analyzing amino acid levels between groups, they did not consider these variables when analyzing gene expression levels between groups; this could potentially lead to biased results if age or PMI had an effect on gene expression levels. Finally, although the authors do mention that they found no significant differences in d-Asp/total Asp ratio between groups in both brain regions after correction for multiple testing was applied; they do not provide any further discussion or explanation for this finding which could be important for understanding the role of glutamatergic signaling in schizophrenia pathophysiology.
In conclusion, overall this article provides a comprehensive overview of glutamatergic alterations in postmortem schizophrenia brains using a multistep approach combining HPLC analysis with qRT-PCR and western blotting analyses. However there are some potential biases that should be taken into consideration when interpreting these results