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DOI | 10.1038/TP.2016.68 | ||||
Año | 2016 | ||||
Tipo | artículo de investigación |
Citas Totales
Autores Afiliación Chile
Instituciones Chile
% Participación
Internacional
Autores
Afiliación Extranjera
Instituciones
Extranjeras
The onset of psychosis is thought to involve interactions between environmental stressors and the brain, with cortisol as a putative mediator. We examined the relationship between the cortisol stress response and brain structure in subjects at ultra-high risk (UHR) for psychosis. Waking salivary cortisol was measured in 22 individuals at UHR for psychosis and 17 healthy controls. Grey matter volume was assessed using magnetic resonance imaging at 3 T. The relationship between the stress response and grey matter volume was investigated using voxel-based analyses. Our predictions of the topography of cortisol action as a structural brain modulator were informed by measures of brain glucocorticoid and mineralcorticoid receptor distribution obtained from the multimodal neuroanatomical and genetic Allen Brain Atlas. Across all subjects, reduced responsivity of the hypothalamus-pituitary-adrenal (HPA) axis was correlated with smaller grey matter volumes in the frontal, parietal and temporal cortex and in the hippocampus. This relationship was particularly marked in the UHR subjects in the right prefrontal, left parahippocampal/fusiform and parietal cortices. The subgroup that subsequently developed psychosis showed a significant blunting of HPA stress response, observed at trend level also in the whole UHR sample. Altered responses to stress in people at high risk of psychosis are related to reductions in grey matter volume in areas implicated in the vulnerability to psychotic disorders. These areas may represent the neural components of a stress vulnerability model.
Ord. | Autor | Género | Institución - País |
---|---|---|---|
1 | Valli, I. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
2 | Crossley, Nicolas | Hombre |
Kings Coll London - Reino Unido
Pontificia Universidad Católica de Chile - Chile King's College London - Reino Unido |
3 | Day, F. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
4 | Stone, J. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
5 | Tognin, S. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
6 | Mondelli, V. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido National Health Service - Reino Unido South London and Maudsley NHS Foundation Trust - Reino Unido |
7 | Howes, O. | - |
Kings Coll London - Reino Unido
Univ London Imperial Coll Sci Technol & Med - Reino Unido King's College London - Reino Unido Imperial College London - Reino Unido |
8 | Valmaggia, L. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
9 | Pariante, C. | - |
Kings Coll London - Reino Unido
King's College London - Reino Unido National Health Service - Reino Unido South London and Maudsley NHS Foundation Trust - Reino Unido |
10 | McGuire, P. | Hombre |
Kings Coll London - Reino Unido
King's College London - Reino Unido |
Fuente |
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Medical Research Council |
NIHR |
Servier |
Lundbeck |
Sunovion |
Pfizer |
AstraZeneca |
National Institute for Health Research |
Eli Lilly and Company |
Eli Lilly |
BMS |
Roche |
Janssen Pharmaceuticals |
Astra-Zeneca |
Roche Products |
Academy of Medical Sciences (AMS) |
Otsuka |
Heptares |
Jansenn |
Rand |
Lyden-Delta |
Autifony |
Sunovion and Hoffman-La Roche |
Pfizer UK |
Agradecimiento |
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JS has received honoraria from Janssen Pharmaceuticals, Behrenberg Bank, AstraZeneca, Pfizer, Sunovion and Hoffman-La Roche. OH has received investigator-initiated research funding from and/or participated in advisory/speaker meetings organised by Astra-Zeneca, Autifony, BMS, Eli Lilly, Heptares, Jansenn, Lundbeck, Lyden-Delta, Otsuka, Servier, Sunovion, Rand and Roche. IV was supported by NIHR clinical lectureship. The remaining authors declare no conflict of interest. |
JS has received honoraria from Janssen Pharmaceuticals, Behrenberg Bank, AstraZeneca, Pfizer, Sunovion and Hoffman-La Roche. OH has received investigator-initiated research funding from and/or participated in advisory/speaker meetings organised by Astra-Zeneca, Autifony, BMS, Eli Lilly, Heptares, Jansenn, Lundbeck, Lyden-Delta, Otsuka, Servier, Sunovion, Rand and Roche. IV was supported by NIHR clinical lectureship. The remaining authors declare no conflict of interest. |