The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex:  A Proteomic Analysis.

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

PROTEOMICS (WEINHEIM. PRINT)

WILEY-V C H VERLAG GMBH

Lugar: Weinheim; Año: 2017 vol. 17

1615-9853

Prenatal iron deficiency (pID) has been described to increase the risk forneurodevelopmental disorders such as autism and schizophrenia; however,the precise molecular mechanisms are still unknown. Here, we utilizedhigh-throughput MS to examine the proteomic effects of pID in adulthood onthe rat frontal cortex area (FCA). In addition, the FCA proteome was examinedin adulthood following risperidone treatment in adolescence to see if theseeffects could be prevented. We identified 1501 proteins of which 100 weresignificantly differentially expressed in the FCA at postnatal day 90. Pathwayanalysis of proteins affected by pID revealed changes in metabolic processes,including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Aktsignaling. Interestingly, most of these protein changes were not present in theadult pID offspring who received risperidone in adolescence. Considering thelink between pID and several neurodevelopmental disorders such as autismand schizophrenia these presented results bring new perspectives tounderstand the role of iron in metabolic pathways and provide novelbiomarkers for future studies of pID.