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Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia
The negative symptoms of schizophrenia, avolition, alogia, apathy and impaired or nonexistent social functioning, are strongly correlated with the progressive course and long-term prognosis of the disease, undermining the patient’s ability to integrate socially, interpersonal skills and quality of l...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2014
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986891/ https://www.ncbi.nlm.nih.gov/pubmed/24670212 http://dx.doi.org/10.1186/1471-244X-14-88 |
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author | Limosin, Frédéric |
author_facet | Limosin, Frédéric |
author_sort | Limosin, Frédéric |
collection | PubMed |
description | The negative symptoms of schizophrenia, avolition, alogia, apathy and impaired or nonexistent social functioning, are strongly correlated with the progressive course and long-term prognosis of the disease, undermining the patient’s ability to integrate socially, interpersonal skills and quality of life. At a time when new drug strategies are being developed, a better understanding of the etiology and pathogenesis underpinning the occurrence of negative symptoms constitutes an essential prerequisite for real therapeutic advances. Approaching this vulnerability from the neurodevelopmental perspective is especially pertinent with regard to the experimental studies conducted in animals. Several models have been put forward, involving a variety of topics such as the deleterious impact of a prenatal infection or of early maternal deprivation on brain development, or else the consequences of trauma and abuse suffered during childhood. These various models are based on biological abnormalities that could guide the identification of new therapeutic targets. They notably include the hyperreactivity of the hypothalamic-pituitary-adrenal axis and dysfunction of corticostriatal glutamatergic transmission. As such, in the traumagenic model, which associates neurodevelopmental and neurodegenerative processes, the dysfunction of corticostriatal glutamatergic transmission, by reducing the tonic dopamine release, could be the cause of an increase in the phasic dopamine release linked to stress. This excessive phasic response to stress may induce cerebral damage by increasing excitotoxicity and oxidative stress. |
format | Online Article Text |
id | pubmed-3986891 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-39868912014-04-16 Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia Limosin, Frédéric BMC Psychiatry Review The negative symptoms of schizophrenia, avolition, alogia, apathy and impaired or nonexistent social functioning, are strongly correlated with the progressive course and long-term prognosis of the disease, undermining the patient’s ability to integrate socially, interpersonal skills and quality of life. At a time when new drug strategies are being developed, a better understanding of the etiology and pathogenesis underpinning the occurrence of negative symptoms constitutes an essential prerequisite for real therapeutic advances. Approaching this vulnerability from the neurodevelopmental perspective is especially pertinent with regard to the experimental studies conducted in animals. Several models have been put forward, involving a variety of topics such as the deleterious impact of a prenatal infection or of early maternal deprivation on brain development, or else the consequences of trauma and abuse suffered during childhood. These various models are based on biological abnormalities that could guide the identification of new therapeutic targets. They notably include the hyperreactivity of the hypothalamic-pituitary-adrenal axis and dysfunction of corticostriatal glutamatergic transmission. As such, in the traumagenic model, which associates neurodevelopmental and neurodegenerative processes, the dysfunction of corticostriatal glutamatergic transmission, by reducing the tonic dopamine release, could be the cause of an increase in the phasic dopamine release linked to stress. This excessive phasic response to stress may induce cerebral damage by increasing excitotoxicity and oxidative stress. BioMed Central 2014-03-26 /pmc/articles/PMC3986891/ /pubmed/24670212 http://dx.doi.org/10.1186/1471-244X-14-88 Text en Copyright © 2014 Limosin; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Limosin, Frédéric Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title | Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title_full | Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title_fullStr | Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title_full_unstemmed | Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title_short | Neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
title_sort | neurodevelopmental and environmental hypotheses of negative symptoms of schizophrenia |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986891/ https://www.ncbi.nlm.nih.gov/pubmed/24670212 http://dx.doi.org/10.1186/1471-244X-14-88 |
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