Antipsychotics, Environmental risk factor, Myelination, Schizophrenia.
Science Foundation Ireland. Grant Number: RFP1304. University of Buenos Aires. Grant Number: UBA 20020100100395.
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 MS 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 postnatal 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 pID 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 pID.
Medicine and Health Sciences | Psychiatry and Psychology
Farrelly L, Rosato-Siri MV, Föcking M, Codagnone M, Reines A, Dicker P, Wynne K, Farrell M, Cannon M, Cagney G, Pasquini JM, Cotter DR. The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex: A Proteomic Analysis. Proteomics. 2017;17(17-18).
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 License.