Artículos de revistas
The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex: A Proteomic Analysis
Fecha
2017-09Registro en:
Farrelly, Lorna; Rosato Siri, María Victoria; Föcking, Melanie; Codagnone, Martín Gabriel; Reines, Analia Gabriela; et al.; The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex: A Proteomic Analysis; Wiley VCH Verlag; Proteomics (weinheim. Print); 17; 17-18; 9-2017; 1-24
1615-9853
CONICET Digital
CONICET
Autor
Farrelly, Lorna
Rosato Siri, María Victoria
Föcking, Melanie
Codagnone, Martín Gabriel
Reines, Analia Gabriela
Dicker, Patrick
Wynne, Kieran
Farrell, Michael
Cannon, Mary
Cagney, Gerard
Pasquini, Juana Maria
Cotter, David R.
Resumen
Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high throughput mass spectrometry to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at post-natal day 90. Pathway Analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Considering the link between prenatal iron deficiency and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of prenatal iron deficiency.