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Neurosci Biobehav Rev. 2015 Feb;49:90-104. doi: 10.1016/j.neubiorev.2014.12.003. Epub 2014 Dec 10.

Fetal programming of schizophrenia: select mechanisms.

Author information

1
Department of Human Genetics, National Institute of Mental Health & Neurosciences, Bangalore 560029, India. Electronic address: monozeet@gmail.com.
2
Translational Psychiatry Laboratory, Neurobiology Research Centre and Department of Psychiatry, National Institute of Mental Health & Neurosciences, Hosur Road, Bangalore 560029, India.
3
IMPACT Strategic Research Centre, School of Medicine, Deakin University, Barwon Health, Geelong, Victoria, Australia; Department of Psychiatry, The Florey Institute of Neuroscience and Mental Health, and Orygen, The National Centre of Excellence in Youth Mental Health, University of Melbourne, Parkville, Australia.

Abstract

Mounting evidence indicates that schizophrenia is associated with adverse intrauterine experiences. An adverse or suboptimal fetal environment can cause irreversible changes in brain that can subsequently exert long-lasting effects through resetting a diverse array of biological systems including endocrine, immune and nervous. It is evident from animal and imaging studies that subtle variations in the intrauterine environment can cause recognizable differences in brain structure and cognitive functions in the offspring. A wide variety of environmental factors may play a role in precipitating the emergent developmental dysregulation and the consequent evolution of psychiatric traits in early adulthood by inducing inflammatory, oxidative and nitrosative stress (IO&NS) pathways, mitochondrial dysfunction, apoptosis, and epigenetic dysregulation. However, the precise mechanisms behind such relationships and the specificity of the risk factors for schizophrenia remain exploratory. Considering the paucity of knowledge on fetal programming of schizophrenia, it is timely to consolidate the recent advances in the field and put forward an integrated overview of the mechanisms associated with fetal origin of schizophrenia.

KEYWORDS:

Diet; Epigenetics; Fetal programming; Infection; Inflammation; Neurodevelopment; Oxidative stress; Perinatal; Prenatal; Schizophrenia; Stress

PMID:
25496904
DOI:
10.1016/j.neubiorev.2014.12.003
[Indexed for MEDLINE]

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