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dc.contributor.authorMöller, M.
dc.contributor.authorSwanepoel, T.
dc.contributor.authorHarvey, B.H.
dc.date.accessioned2016-08-19T11:04:59Z
dc.date.available2016-08-19T11:04:59Z
dc.date.issued2015
dc.identifier.citationMöller, M. et al. 2015. Neurodevelopmental animal models reveal the convergent role of neurotransmitter systems, inflammation, and oxidative stress as biomarkers of schizophrenia: implications for novel drug development. ACS chemical neuroscience, 6(7): 987-1016. [https://doi.org/10.1021/cn5003368]en_US
dc.identifier.issn1948-7193 (Online)
dc.identifier.urihttp://hdl.handle.net/10394/18337
dc.identifier.urihttps://pubs.acs.org/doi/10.1021/cn5003368
dc.identifier.urihttps://doi.org/10.1021/cn5003368
dc.description.abstractSchizophrenia is a life altering disease with a complex etiology and pathophysiology, and although antipsychotics are valuable in treating the disorder, certain symptoms and/or sufferers remain resistant to treatment. Our poor understanding of the underlying neuropathological mechanisms of schizophrenia hinders the discovery and development of improved pharmacological treatment, so that filling these gaps is of utmost importance for an improved outcome. A vast amount of clinical data has strongly implicated the role of inflammation and oxidative insults in the pathophysiology of schizophrenia. Preclinical studies using animal models are fundamental in our understanding of disease development and pathology as well as the discovery and development of novel treatment options. In particular, social isolation rearing (SIR) and pre- or postnatal inflammation (PPNI) have shown great promise in mimicking the biobehavioral manifestations of schizophrenia. Furthermore, the “dual-hit” hypothesis of schizophrenia states that a first adverse event such as genetic predisposition or a prenatal insult renders an individual susceptible to develop the disease, while a second insult (e.g., postnatal inflammation, environmental adversity, or drug abuse) may be necessary to precipitate the full-blown syndrome. Animal models that emphasize the “dual-hit” hypothesis therefore provide valuable insight into understanding disease progression. In this Review, we will discuss SIR, PPNI, as well as possible “dual-hit” animal models within the context of the redox-immune-inflammatory hypothesis of schizophrenia, correlating such changes with the recognized monoamine and behavioral alterations of schizophrenia. Finally, based on these models, we will review new therapeutic options, especially those targeting immune-inflammatory and redox pathwaysen_US
dc.description.sponsorshipSouth African Medical Research Councilen_US
dc.language.isoenen_US
dc.publisherACSen_US
dc.subjectRedox-immune-inflammatoryen_US
dc.subjectSocial isolation rearingen_US
dc.subjectInflammation modelsen_US
dc.subject“Dual-hit” modelsen_US
dc.subjectSchizophreniaen_US
dc.subjectMonoaminesen_US
dc.titleNeurodevelopmental animal models reveal the convergent role of neurotransmitter systems, inflammation, and oxidative stress as biomarkers of schizophrenia: implications for novel drug developmenten_US
dc.typeArticleen_US
dc.contributor.researchID21247250 - Möller Wolmarans, Marisa
dc.contributor.researchID21700486 - Swanepoel, Twanette
dc.contributor.researchID11083417 - Harvey, Brian Herbert


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