Accessing Gene Expression in Treatment-Resistant Schizophrenia.

摘要: Schizophrenia (SCZ) is a mental disorder arising from complex interaction of genetic and environmental factors. It has been suggested that treatment-resistant schizophrenia (TRS) distinct, more severe, homogenous subgroup could present specific biological markers. Our aim was to characterize expression target genes in blood TRS patients compared with non-TRS (NTRS) healthy controls (HC). defined using failure respond two previous antipsychotic trials. We hypothesized involved neurodevelopment, myelination, neuroplasticity, neurotransmission, miRNA processing be treatment resistance; then, we investigated 13 related those processes 256 subjects, being 94 162 treated antipsychotics. Of those, 78 were 84 NTRS patients. Peripheral samples collected all subjects RNA isolated. Gene analysis performed the TaqMan low-density array (TLDA) technology. To verify influence quantitative trait loci (eQTLs), evaluated single-nucleotide polymorphism (SNP) data GTEx Project. SNP genotypes obtained HumanOmniExpress BeadChip. did not detect gene differences between indicating candidate resistance. detected an upregulation CNR1 UFD1L (TRS groups) when controls, may associated release neurotransmitters, which can neuronal plasticity, or stress response-activating protein degradation. DICER1 AKT1 increased slightly across groups differentiate only extreme opposite groups, HC TRS. Both act heterogeneous pathways, such as cell signaling processing, seem have demand group. any eQTLs our sample explain mRNA levels, suggesting possible regulation by other mechanism, driven genotypes. strengthen importance several pathways refractoriness severity, adding knowledge develop effective treatments future.