Hormones and schizophrenia

Kulkarni, Jayashri; Hayes, Emily; Gavrilidis, Emorfia

doi:10.1097/yco.0b013e328350360e

Cited by 68 publications

(47 citation statements)

References 64 publications

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“…This smoother course of the disorder associated to a later onset of the frank episode of psychosis was attributed to the protective effects of estrogens in women (Reicher-Rossler et al, 1994;Seeman and Lang, 1990;Kulkarni et al, 2012). An older age of onset also allows the development of social skills and experience, and favors better coping with the difficulties and problems generated by the disorder and its consequences.…”

Section: Clinical Implications Of the Findingsmentioning

confidence: 94%

“…Alcohol and drug abuse appeared significantly more often among men, impacting on social functioning (Køster et al, 2008). Conversely, estrogens were supposed to modulate dopaminergic hyperactivity in females, thus leading to a smoother course of the disorder and a later onset of the frank episode of psychosis (Reicher-Rossler et al, 1994;Seeman and Lang, 1990;Kulkarni et al, 2012).…”

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

Sex differences in first-episode psychosis and in people at ultra-high risk

Cocchi¹,

Lora²,

Meneghelli³

et al. 2014

Psychiatry Research

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Section: Clinical Implications Of the Findingsmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 96%

Sex differences in first-episode psychosis and in people at ultra-high risk

Cocchi¹,

Lora²,

Meneghelli³

et al. 2014

Psychiatry Research

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“…Consistently, while we demonstrated that Rasd2-targeted deletion prominently enhanced Amphand PCP-induced motor stimulation in both genders, we found that knockout females were protected against PPI dysfunction, seen in males. Given the established role of estrogen hormones in regulating the onset and severity of symptoms in patients with schizophrenia (Kulkarni et al, 2012), the gender-dependent PPI responses found in Rasd2 mutants represent an intriguing translational feature to decipher in future experiments. Accordingly, this preclinical model may provide a valuable in vivo tool to unveil the molecular determinants underlying the obscure interaction among sexual hormones and sensorimotor gating processes reported in humans (Kumari, 2011).…”

Section: Rasd2 Regulates Psychotomimetic Drug Effects D Vitucci Et Almentioning

confidence: 99%

Rasd2 Modulates Prefronto-Striatal Phenotypes in Humans and ‘Schizophrenia-Like Behaviors’ in Mice

Vitucci

Giorgio

Napolitano

et al. 2015

Neuropsychopharmacol

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Rasd2 is a thyroid hormone target gene, which encodes for a GTP-binding protein enriched in the striatum where, among other functions, it modulates dopaminergic neurotransmission. Here we report that human RASD2 mRNA is abundant in putamen, but it also occurs in the cerebral cortex, with a distinctive expression pattern that differs from that present in rodents. Consistent with its localization, we found that a genetic variation in RASD2 (rs6518956) affects postmortem prefrontal mRNA expression in healthy humans and is associated with phenotypes of relevance to schizophrenia, including prefrontal and striatal grey matter volume and physiology during working memory, as measured with magnetic resonance imaging. Interestingly, quantitative real-time PCR analysis indicated that RASD2 mRNA is slightly reduced in postmortem prefrontal cortex of patients with schizophrenia. In the attempt to uncover the neurobiological substrates associated with Rasd2 activity, we used knockout mice to analyze the in vivo influence of this G-protein on the prepulse inhibition of the startle response and psychotomimetic drug-related behavioral response. Data showed that Rasd2 mutants display deficits in basal prepulse inhibition that, in turn, exacerbate gating disruption under psychotomimetic drug challenge. Furthermore, we documented that lack of Rasd2 strikingly enhances the behavioral sensitivity to motor stimulation elicited by amphetamine and phencyclidine. Based on animal model data, along with the finding that RASD2 influences prefronto-striatal phenotypes in healthy humans, we suggest that genetic mutation or reduced levels of this G-protein might have a role in cerebral circuitry dysfunction underpinning exaggerated psychotomimetic drugs responses and development of specific biological phenotypes linked to schizophrenia.

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“…Hormones have also been linked to the occurrence of schizophrenia, with oestrogen being protective (for a review see Kulkarni, Hayes, & Gavrilidis, 2012). Second, sex differences in interhemispheric transfer may provide an explanation (e.g., Nowicka & Fernsten, 2001).…”

Section: Bourne and Mckaymentioning

confidence: 99%

Paranoid males have reduced lateralisation for processing of negative emotions: An investigation using the chimeric faces test

Bourne

McKay

2013

Laterality: Asymmetries of Body, Brain and Cognition

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Reduced strength of lateralisation in patients with schizophrenia has been reported in a number of studies. However the exact nature of this relationship remains unclear. In this study, lateralisation for processing emotional faces was measured using the chimeric faces test and examined in relation to paranoia in a non-clinical sample. For males only, those with higher scores on a paranoia questionnaire had reduced lateralisation for processing negative facial emotion. For females there were no significant relationships. These findings suggest that atypical patterns of lateralisation for processing emotional stimuli may be implicated in, or associated with, increased levels of paranoia.

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Hormones and schizophrenia

Cited by 68 publications

References 64 publications

Sex differences in first-episode psychosis and in people at ultra-high risk

Sex differences in first-episode psychosis and in people at ultra-high risk

Rasd2 Modulates Prefronto-Striatal Phenotypes in Humans and ‘Schizophrenia-Like Behaviors’ in Mice

Paranoid males have reduced lateralisation for processing of negative emotions: An investigation using the chimeric faces test

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