dc.contributor.author | Möller, M. | |
dc.contributor.author | Swanepoel, T. | |
dc.contributor.author | Harvey, B.H. | |
dc.date.accessioned | 2016-08-19T11:04:59Z | |
dc.date.available | 2016-08-19T11:04:59Z | |
dc.date.issued | 2015 | |
dc.identifier.citation | Möller, 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.issn | 1948-7193 (Online) | |
dc.identifier.uri | http://hdl.handle.net/10394/18337 | |
dc.identifier.uri | https://pubs.acs.org/doi/10.1021/cn5003368 | |
dc.identifier.uri | https://doi.org/10.1021/cn5003368 | |
dc.description.abstract | Schizophrenia 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 pathways | en_US |
dc.description.sponsorship | South African Medical Research Council | en_US |
dc.language.iso | en | en_US |
dc.publisher | ACS | en_US |
dc.subject | Redox-immune-inflammatory | en_US |
dc.subject | Social isolation rearing | en_US |
dc.subject | Inflammation models | en_US |
dc.subject | “Dual-hit” models | en_US |
dc.subject | Schizophrenia | en_US |
dc.subject | Monoamines | en_US |
dc.title | Neurodevelopmental animal models reveal the convergent role of neurotransmitter systems, inflammation, and oxidative stress as biomarkers of schizophrenia: implications for novel drug development | en_US |
dc.type | Article | en_US |
dc.contributor.researchID | 21247250 - Möller Wolmarans, Marisa | |
dc.contributor.researchID | 21700486 - Swanepoel, Twanette | |
dc.contributor.researchID | 11083417 - Harvey, Brian Herbert | |