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The Effects of Prenatal Iron Deficiency and Risperidone Treatment on the Rat Frontal Cortex: A Proteomic Analysis
Lorna Farrelly1, Maria Victoria Rosato-Siri2, Melanie Föcking1
1Department of Psychiatry, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin, Ireland.
Insights
Prenatal iron deficiency (pID) alters adult brain proteomes, impacting metabolic pathways. Adolescent risperidone treatment may prevent these neurodevelopmental changes, offering new insights into iron
Area of Science:
- Neuroscience
- Biochemistry
- Developmental Biology
Background:
- Prenatal iron deficiency (pID) is linked to neurodevelopmental disorders like autism and schizophrenia.
- The molecular mechanisms underlying this association remain unclear.
- Iron's role in brain development and function is critical.
Purpose of the Study:
- To investigate the proteomic consequences of prenatal iron deficiency in the adult rat frontal cortex.
- To determine if adolescent risperidone treatment can mitigate these proteomic changes.
- To explore potential molecular pathways affected by pID.
Main Methods:
- High-throughput mass spectrometry (MS) was used to analyze the proteome of the rat frontal cortex area (FCA).
- Proteins were quantified and compared between control and pID groups.
- Pathway analysis was performed on differentially expressed proteins.
Main Results:
- 1501 proteins were identified in the FCA, with 100 significantly altered in pID rats at postnatal day 90.
- Affected pathways included the tricarboxylic acid cycle, mitochondrial dysfunction, and PI3K/Akt signaling.
- Most protein alterations were absent in pID offspring treated with risperidone during adolescence.
Conclusions:
- Prenatal iron deficiency induces significant proteomic changes in the adult rat frontal cortex, affecting key metabolic and signaling pathways.
- Adolescent risperidone treatment shows potential in preventing or reversing these pID-induced molecular alterations.
- These findings offer new perspectives on iron's role in neurodevelopment and suggest potential biomarkers for pID-related neurodevelopmental disorders.
Abstract:
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.
