Carmine M Pariante

King's College London, Londinium, England, United Kingdom

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Publications (232)1010.24 Total impact

  • David Baumeister, Stafford L Lightman, Carmine M Pariante
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    ABSTRACT: Abnormalities of hypothalamic-pituitary-adrenal (HPA) axis function are one of the most consistent biological findings across several mental disorders, but many of the mechanisms underlying this abnormality as well as the potential contribution to behavioural phenotypes remain only partially understood. Interestingly, evidence suggests a U-curve, with dysregulation of the HPA axis towards both hyper- or hypoactivity manifesting as a risk to mental wellbeing. This review will elaborate on both the clinical and molecular role of the neuroendocrine stress system in depressive, psychotic and post-traumatic stress disorders and present some of the most recent findings that have shed light on the complex interface between environmental stressors, molecular mechanisms and clinical presentation. Crucially, plasticity of the HPA axis confers both vulnerability to adverse events, particularly so in early developmental stages, as well as hope for the treatment of mental disorder, as evidenced by changes in HPA functioning associated with remission of symptoms.
    Current topics in behavioral neurosciences. 03/2014;
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    ABSTRACT: Psychological stress is implicated in the development of schizophrenia, but little is known about experiences of stress among children at elevated risk for the disorder. To examine stressor exposure and reactivity in children with different vulnerability profiles for schizophrenia: (a) children presenting multiple antecedents of schizophrenia (ASz group), (b) children with a family history of schizophrenia (FHx group) and (c) typically developing low-risk (TD) children. Ninety-five children (ASz = 29; FHx = 19; ASz+FHx = 5; TD = 42), identified aged 9-12 years using a community-based screening procedure or as relatives of individuals with schizophrenia, completed questionnaires assessing environmental stressors and psychopathology at age 11-14 years. Relative to their typically developing peers, children in the FHx and ASz groups were exposed to a greater number of negative life events and a higher frequency of daily stressors, respectively; and were more distressed by these experiences. Stress exposure and reactivity may constitute useful targets of early intervention for psychosis.
    The British journal of psychiatry: the journal of mental science 03/2014; · 6.62 Impact Factor
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    ABSTRACT: Background Interferon (IFN)-α therapy for chronic hepatitis C virus (HCV) infection is frequently associated with depression. The routine prophylaxis with antidepressants might expose patients to adverse effects, hence the need for alternative preventive interventions. Omega-3 polyunsaturated fatty acids (PUFAs) are safe and effective essential nutritional compounds used for the treatment of depression, putatively through an anti-inflammatory action. In addition, lower erythrocyte levels of omega-3 PUFA have been associated with an increased risk of IFN-induced depression. Methods We conducted a 2-week, double-blind, placebo-controlled trial, comparing eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and placebo, for the prevention of IFN-α-induced depression. A total of 162 patients consented to participate and were randomized to the study, and all of them completed the two-week trial; 152 participants were followed throughout the 24 weeks of IFN-α treatment, and were included in the analysis. Results Compared with placebo, the incident rates of IFN-α-induced depression were significantly lower in EPA-, but not in DHA-treated patients (10% and 28%, respectively, vs. 30% for placebo, P=0.037). Both EPA and DHA significantly delayed the onset of IFN-induced depression (week of onset: 12.0 and 11.7, respectively, vs. 5.3 for placebo, P=0.002). EPA and DHA were both well tolerated in this population. EPA treatment increased both EPA and DHA erythrocyte levels, but DHA only increased DHA erythrocyte levels. Conclusions EPA is effective in the prevention of depression in HCV patients received IFN-α therapy. Our study confirms the notion that anti-inflammatory strategies are effective antidepressants in the context of depression associated with inflammation.
    Biological psychiatry 01/2014; · 8.93 Impact Factor
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    ABSTRACT: Abnormal hypothalamic-pituitary-adrenal (HPA) axis function, as indexed by elevated diurnal cortisol levels and/or a blunted cortisol awakening response (CAR), has been observed among patients with first episode psychosis and associated with neurocognitive deficits in this population. However, the extent to which these features precede illness onset is unclear. The current study aimed to determine whether children who are at putatively elevated risk for psychosis because they present multiple antecedents of schizophrenia (ASz), and high-risk children with a family history of illness (FHx), are characterised by abnormal cortisol levels when compared with their typically-developing (TD) peers. A further aim was to investigate the extent to which cortisol levels are associated with psychosocial stress and neurocognitive function. Thirty-three ASz children, 22 FHx children, and 40 TD children were identified at age 9-12 years using a novel community-based screening procedure or as relatives of individuals with schizophrenia. All participants were antipsychotic-naive and not currently seeking treatment for their symptoms. At age 11-14 years, participants provided salivary cortisol samples and completed psychosocial stress measures and tests of memory and executive function. Results indicated that FHx children, but not ASz children, were characterised by a blunted CAR relative to their TD peers (effect size = 0.73, p = 0.01) that was not explained by psychosocial stress exposure or by distress relating to these experiences. Neither FHx nor ASz children were characterised by elevated diurnal cortisol. Among both FHx and ASz children, more pronounced HPA axis function abnormalities (i.e., higher diurnal cortisol levels and greater blunting of the CAR) were associated with poorer performance on tests of verbal memory and executive function. These findings support the notion that at least some HPA axis abnormalities described in psychosis precede illness onset, rather than being a subsequent epiphenomenon. We speculate that the blunted CAR may constitute an early (potentially genetically-mediated) marker of psychosis vulnerability, whilst elevated diurnal cortisol levels may emerge only proximally to disease onset.
    Psychoneuroendocrinology 01/2014; · 5.14 Impact Factor
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    ABSTRACT: Objective: To carry out a systematic review of the literature addressing cognitive functions in first-episode psychosis (FEP), divided into domains. Although this is not a full "cognitive-genetics-in-schizophrenia review," we will also include putative ideas of mechanism(s) behind these impairments, focusing on how early stress, and genetic vulnerability may moderate cognitive function in psychosis. Method: Relevant studies were identified via computer literature searches for research published up to and including January 2013, only case-control studies were included for the neurocognitive meta-analysis. Results: Patients with FEP present global cognitive impairment compared to healthy controls. The largest effect size was observed for verbal memory (Cohen's d effect size = 2.10), followed by executive function (effect size = 1.86), and general IQ (effect size = 1.71). However, effect sizes varied between studies. Conclusion: Cognitive impairment across domains, up to severe level based on Cohen's effect size, is present already in FEP studies. However, differences in levels of impairment are observed between studies, as well as within domains, indicating that further consolidation of cognitive impairment over the course of illness may be present. Cognitive abnormalities may be linked to a neurodevelopmental model including increased sensitivity to the negative effect of stress, as well as genetic vulnerability. More research on this field is needed.
    Frontiers in Psychiatry 01/2014; 4:182.
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    ABSTRACT: axis and aging in depression: systematic review and meta-analysis, Psychoneuroendocrinology (2013), This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
    Psychoneuroendocrinology 12/2013; · 5.14 Impact Factor
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    ABSTRACT: Cannabis use is associated with an earlier age of onset of psychosis (AOP). However, the reasons for this remain debated. Methods: We applied a Cox proportional hazards model to 410 first-episode psychosis patients to investigate the association between gender, patterns of cannabis use, and AOP. Results: Patients with a history of cannabis use presented with their first episode of psychosis at a younger age (mean years = 28.2, SD = 8.0; median years = 27.1) than those who never used cannabis (mean years = 31.4, SD = 9.9; median years = 30.0; hazard ratio [HR] = 1.42; 95% CI: 1.16-1.74; P < .001). This association remained significant after controlling for gender (HR = 1.39; 95% CI: 1.11-1.68; P < .001). Those who had started cannabis at age 15 or younger had an earlier onset of psychosis (mean years = 27.0, SD = 6.2; median years = 26.9) than those who had started after 15 years (mean years = 29.1, SD = 8.5; median years = 27.8; HR = 1.40; 95% CI: 1.06-1.84; P = .050). Importantly, subjects who had been using high-potency cannabis (skunk-type) every day had the earliest onset (mean years = 25.2, SD = 6.3; median years = 24.6) compared to never users among all the groups tested (HR = 1.99; 95% CI: 1.50- 2.65; P < .0001); these daily users of high-potency cannabis had an onset an average of 6 years earlier than that of non-cannabis users. Conclusions: Daily use, especially of high-potency cannabis, drives the earlier onset of psychosis in cannabis users.
    Schizophrenia Bulletin 12/2013; · 8.80 Impact Factor
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    ABSTRACT: Abstract Background: Treatment-resistant depression patients show both reduced glucocorticoid receptor function and a hyperactive hypothalamic-pituitary- adrenal axis. However, few studies have examined the role of the mineralocorticoid receptor. This study aimed to evaluate the functional activity of the mineralocorticoid receptor system in regulating the hypothalamic-pituitary-adrenal axis in well-defined treatment-resistant depression patients. Material and method: We recruited 24 subjects divided into: (a) treatment-resistant depression; (b) healthy controls. We evaluated: (a) the effect of combined glucocorticoid receptor mineralocorticoid receptor stimulation with prednisolone; (b) the effect of prednisolone with the mineralocorticoid receptor antagonist spironolactone; and (c) the effect of spironolactone alone. The response of the hypothalamic-pituitary-adrenal axis was measured using salivary cortisol and plasma levels of drugs were also measured. Results: Treatment-resistant depression patients had higher cortisol compared with controls after all challenges. In controls, spironolactone increased cortisol compared to placebo. The co-administration of spironolactone with prednisolone in controls decreases the suppressive effects of prednisolone. In contrast, in treatment-resistant depression, spironolactone did not increase cortisol compared to placebo and spironolactone with prednisolone had no effect on the suppressive effects of prednisolone. Patients with treatment-resistant depression had a reduction in the conversation of spironolactone to the active metabolite canrenone. Conclusion: Our data confirmed that treatment-resistant depression is associated with hypercortisolism and these patients no longer show an hypothalamic-pituitary-adrenal response to the administration of a mineralocorticoid receptor antagonist, suggesting that there is a mineralocorticoid receptor malfunctioning, such as a down regulation, however, pharmacokinetics and pharmacodynamics in these subjects could also have had an effect on the lack of mineralocorticoid receptor response
    Journal of Psychopharmacology 12/2013; · 3.37 Impact Factor
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    ABSTRACT: The integrity of brain white matter connections is central to a patient's ability to respond to pharmacological interventions. This study tested this hypothesis using a specific measure of white matter integrity, and examining its relationship to treatment response using a prospective design in patients within their first episode of psychosis. Diffusion tensor imaging data were acquired in 63 patients with first episode psychosis and 52 healthy control subjects (baseline). Response was assessed after 12 weeks and patients were classified as responders or non-responders according to treatment outcome. At this second time-point, they also underwent a second diffusion tensor imaging scan. Tract-based spatial statistics were used to assess fractional anisotropy as a marker of white matter integrity. At baseline, non-responders showed lower fractional anisotropy than both responders and healthy control subjects (P < 0.05; family-wise error-corrected), mainly in the uncinate, cingulum and corpus callosum, whereas responders were indistinguishable from healthy control subjects. After 12 weeks, there was an increase in fractional anisotropy in both responders and non-responders, positively correlated with antipsychotic exposure. This represents one of the largest, controlled investigations of white matter integrity and response to antipsychotic treatment early in psychosis. These data, together with earlier findings on cortical grey matter, suggest that grey and white matter integrity at the start of treatment is an important moderator of response to antipsychotics. These findings can inform patient stratification to anticipate care needs, and raise the possibility that antipsychotics may restore white matter integrity as part of the therapeutic response.
    Brain 11/2013; · 9.92 Impact Factor
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    ABSTRACT: Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both highly prevalent conditions associated with extreme disability and with the development of co-morbid psychiatric disorders, such as depression and anxiety. Childhood stressors have been shown to induce persistent changes in the function of biological systems potentially relevant to the pathogenesis of both CFS and FM, such as the inflammatory system and the hypothalamic-pituitary-adrenal (HPA) axis. In this review, we examined whether multiple forms of childhood stressors are contributing factors to the development of these disorders, and of the associated psychiatric symptoms. Using PubMed, we identified 31 papers relevant to this narrative review. We included cohort studies and case-control studies, without any exclusion in terms of age and gender. No study characteristics or publication date restrictions were imposed. Most studies across the literature consistently show that there is a strong association between experiences of childhood stressors and the presence of CFS and FM, with rates of CFS/FM being two- to three-fold higher in exposed than in unexposed subjects. We also found evidence for an increased risk for the development of additional symptoms, such as depression, anxiety and pain, in individuals with CFS and FM with a previous history of childhood stressors, compared with individuals with CFS/FM and no such history. Our review confirms that exposure to childhood stressors is associated with the subsequent development of fatigue syndromes such as CFS and FM, and related symptoms. Further studies are needed to identify the mechanisms underlying these associations.
    Psychological Medicine 10/2013; · 5.59 Impact Factor
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    ABSTRACT: IMPORTANCE At present, no reliable predictors exist to distinguish future responders from nonresponders to treatment during the first episode of psychosis. Among potential neuroimaging predictors of treatment response, gyrification represents an important marker of the integrity of normal cortical development that may characterize, already at illness onset, a subgroup of patients with particularly poor outcome. OBJECTIVE To determine whether patients with first-episode psychosis who do not respond to 12 weeks of antipsychotic treatment already have significant gyrification defects at illness onset. DESIGN Case-control study with 12 weeks' longitudinal follow-up to determine treatment response. SETTING Secondary psychiatric services in an inner-city area (South London, England). PARTICIPANTS A total of 126 subjects, including 80 patients presenting with first-episode psychosis and 46 healthy controls. Patients were scanned at the outset and received various antipsychotic medications in a naturalistic clinical setting. They were followed up for 12 weeks and classified as responders or nonresponders if they reached criteria for symptom remission, evaluated with the Psychiatric and Personal History Schedule. OBSERVATION Patients were exposed to naturalistic antipsychotic treatment for 12 weeks following a magnetic resonance imaging scan. MAIN OUTCOMES AND MEASURES Cortical gyrification was assessed using local gyrification index in a vertexwise fashion across the entire cortical surface with correction for multiple testing using permutation analysis. Differences in local gyrification index were assessed between responders, nonresponders, and healthy controls. The effect of diagnosis (affective vs nonaffective psychosis) on the local gyrification index was also investigated in responders and nonresponders. RESULTS Patients with first-episode psychosis showed a significant reduction in gyrification (hypogyria) across multiple brain regions compared with healthy controls. Interestingly, nonresponders showed prominent hypogyria at bilateral insular, left frontal, and right temporal regions when compared with responders (all clusters significant at P < .05). These effects were present for both affective and nonaffective psychoses. CONCLUSIONS AND RELEVANCE Gyrification appears to be a useful predictor of antipsychotic treatment response. Early neurodevelopmental aberrations may predict unfavorable prognosis in psychosis, irrespective of the existing diagnostic boundaries.
    JAMA Psychiatry 08/2013; · 12.01 Impact Factor
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    ABSTRACT: Individuals with psychotic disorders are more likely to have vitamin D (VD) deficiency, while evidence suggests VD could have pathophysiological roles. We summarized meta-analytically the available evidence on VD levels in psychotic disorders in comparison with healthy controls and other psychiatric illnesses. We found seven studies, all reporting insufficient VD levels in patients with psychosis. Schizophrenia had a medium effect size for lower VD than healthy controls, and a trend for lower levels than other psychoses. There were non-significant differences between schizophrenia and major depression. No study has investigated the potential psychotropic effects of VD supplementation in patients with psychosis.
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    ABSTRACT: Individuals with psychotic disorders are more likely to have vitamin D (VD) deficiency, while evidence suggests VD could have pathophysiological roles. We summarized meta-analytically the available evidence on VD levels in psychotic disorders in comparison with healthy controls and other psychiatric illnesses. We found seven studies, all reporting insufficient VD levels in patients with psychosis. Schizophrenia had a medium effect size for lower VD than healthy controls, and a trend for lower levels than other psychoses. There were non-significant differences between schizophrenia and major depression. No study has investigated the potential psychotropic effects of VD supplementation in patients with psychosis.
    Schizophrenia Research 07/2013; · 4.59 Impact Factor
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    ABSTRACT: A larger pituitary size is thought to reflect a greater activation of the hypothalamic-pituitary-adrenal (HPA) axis, which may be related to an increase in the number and size of corticotroph cells. Some studies, but not all, indicate that pituitary volume increases before or at the onset of psychosis. There is a need for at critical appraisal of the literature on this topic accompanied by a meta-analytical evaluation of the data. We included studies comparing the volume of the pituitary gland in healthy controls and patients with schizophrenia, first episode of psychosis (FEP), schizotypal disorder or ultra high-risk (UHR) subjects. We defined three groups of subjects for the analyses: healthy controls; UHR and schizotypal patients; and patients diagnosed with first episode of psychosis, schizophrenia or schizoaffective disorder. Ten studies were included in the meta-analysis. We found a trend of a larger pituitary volume in both UHR subject who had transition to psychosis (p=0.05) and in FEP subjects (p=0.09) compared to healthy controls. There was no difference in pituitary volume between patients with schizophrenia combined with FEP versus healthy controls (p=0.52) or between UHR (with and without transition) and healthy controls (p=0.24). In a regression analysis, we demonstrated that the number of subjects receiving antipsychotics and pituitary volume were positively correlated. As previously reported in other samples, gender also had an impact on pituitary volume with females presenting with a larger mean volume. Results from this meta-analysis suggest that the pituitary gland could be increasing before the onset of psychosis. Both gender and use of antipsychotics have a major impact on the pituitary volume.
    Psychoneuroendocrinology 07/2013; · 5.14 Impact Factor
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    ABSTRACT: Despite increasing evidence suggesting that childhood maltreatment is significantly associated with psychosis, the specific role of bullying in the onset of psychotic disorders is still unclear. This study aimed to examine whether bullying was more prevalent amongst individuals presenting to services for the first time with a psychotic disorder than in unaffected community controls. Data on exposure to bullying, psychotic symptoms, cannabis use and history of conduct disorder were collected cross-sectionally from 222 first-presentation psychosis cases and 215 geographically-matched controls. Bullying victimisation was assessed retrospectively as part of the Brief Life Events schedule. Logistic regression was used to examine associations between exposure to bullying and case-control status, while controlling for potential confounders. Psychosis cases were approximately twice as likely to report bullying victimisation when compared to controls. No significant interactions between bullying and either gender or cannabis use were found. Controls reporting being a victim of bullying were approximately twice as likely to also report at least one psychosis-like symptom. Our results extend previous research by suggesting that bullying victimisation may contribute to vulnerability to develop a psychotic disorder in some individuals.
    Schizophrenia Research 07/2013; · 4.59 Impact Factor
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    ABSTRACT: Major depressive disorder is an extremely debilitating condition affecting millions of people worldwide. Nevertheless, currently available antidepressant medications still have important limitations, such as a low response rate and a time lag for treatment response that represent a significant problem when dealing with individuals who are vulnerable and prone to self-harm. Recent clinical trials have shown that the N-methyl-D-aspartate receptor antagonist, ketamine, can induce an antidepressant response within hours, which lasts up to 2 weeks, and is effective even in treatment-resistant patients. Nonetheless, its use is limited due to its psychotomimetic and addictive properties. Understanding the molecular pathways through which ketamine exerts its antidepressant effects would help in the developing of novel antidepressant agents that do not evoke the same negative side effects of this drug. This review focuses specifically on the effects of ketamine on three molecular mechanisms that are relevant to depression: synaptogenesis, immunomodulation and regulation of glycogen synthase kinase-3 activity.Molecular Psychiatry advance online publication, 23 July 2013; doi:10.1038/mp.2013.87.
    Molecular psychiatry 07/2013; · 15.05 Impact Factor
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    ABSTRACT: Maternal severe mental illness (SMI) disrupts mother-infant interaction in the immediate postpartum and is associated with less than optimal offspring development. In-patient mother and baby units (MBUs) provide the opportunity of supporting mothers with SMI in developing their relationships with their infants in order to minimise this disruption. One way is through an individualised video feedback intervention, delivered as part of a multidisciplinary inpatient treatment package. The present study prospectively measured changes in mother-infant interaction following video feedback intervention, during admission to an MBU (N = 49). Comparisons were made with mother-infant interactions of (1) a community-based ill group of mothers (N = 67) with a mental health diagnosis of similar severity, living at home and without the intervention and (2) a group of healthy mothers (N = 22). Maternal sensitivity and unresponsiveness, and infant cooperativeness and passiveness, were measured from a 3-min videotaped play session, using the CARE-Index. Following admission and the video feedback intervention, the MBU mothers (irrespective of diagnosis) and their infants showed improvements in their interactions. Moreover, on discharge the MBU dyads were significantly more sensitive, cooperative and responsive than the community ill group, and as attuned as the healthy group. While the design of the study does not allow us to conclude unequivocally that the video feedback intervention has effects on the outcome for the mothers and babies independent from the whole inpatient therapeutic package, the results do show that the dyadic interaction of mothers with SMI and their infants improves following the focussed treatment package in a specialised MBU.
    Journal of psychiatric research 06/2013; · 3.72 Impact Factor
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    ABSTRACT: Context:Cross-sectional studies of the signs and symptoms of psychosis yield dimensional phenotypes. However, the validity and clinical utility of such dimensions remain debated. This study investigated the structure of psychotic symptomatology, the stability of the structure over time, and the concordance between symptom dimensions and categorical diagnoses.Methods:Sample consisted of 500 first-episode psychotic patients. A cross-sectional study (N = 500) investigated the organizational structure of symptom dimensions at the onset of psychosis and its concordance with categorical diagnoses; next, a nested longitudinal study (N = 100) examined the stability of the symptom dimensions structure after 5-10 years of follow-up.Results:Factor analyses identified 6 first-order factors (mania, negative, disorganization, depression, hallucinations, and delusions) and 2 high-order factors (affective and nonaffective psychoses). Cumulative variance accounted for by the first and high-order factors was 63%: 31% by the first-order factors and 32% by the high-order factors. The factorial structure of psychotic symptoms during first episode remained stable after 5-10 years of follow-up. The overall concordance between 4 categorical diagnostic groups (schizophrenia, mania with psychosis, psychotic depression and schizoaffective disorder) and dimensional symptom ranged from 62.2% to 73.1% (when the schizoaffective group was excluded).Conclusions:Symptoms of psychosis assume a multidimensional hierarchical structure. This hierarchical model was stable over time and showed good concordance with categorical diagnoses. The combined use of dimensional and categorical approach to psychotic disorders would be of clinical and research utility.
    Schizophrenia Bulletin 05/2013; · 8.80 Impact Factor
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    ABSTRACT: Stress and glucocorticoid hormones regulate hippocampal neurogenesis, but the molecular mechanisms mediating these effects are poorly understood. Here we identify the glucocorticoid receptor (GR) target gene, serum- and glucocorticoid-inducible kinase 1 (SGK1), as one such mechanism. Using a human hippocampal progenitor cell line, we found that a small molecule inhibitor for SGK1, GSK650394, counteracted the cortisol-induced reduction in neurogenesis. Moreover, gene expression and pathway analysis showed that inhibition of the neurogenic Hedgehog pathway by cortisol was SGK1-dependent. SGK1 also potentiated and maintained GR activation in the presence of cortisol, and even after cortisol withdrawal, by increasing GR phosphorylation and GR nuclear translocation. Experiments combining the inhibitor for SGK1, GSK650394, with the GR antagonist, RU486, demonstrated that SGK1 was involved in the cortisol-induced reduction in progenitor proliferation both downstream of GR, by regulating relevant target genes, and upstream of GR, by increasing GR function. Corroborating the relevance of these findings in clinical and rodent settings, we also observed a significant increase of SGK1 mRNA in peripheral blood of drug-free depressed patients, as well as in the hippocampus of rats subjected to either unpredictable chronic mild stress or prenatal stress. Our findings identify SGK1 as a mediator for the effects of cortisol on neurogenesis and GR function, with particular relevance to stress and depression.
    Proceedings of the National Academy of Sciences 05/2013; · 9.74 Impact Factor

Publication Stats

5k Citations
1,010.24 Total Impact Points


  • 2001–2014
    • King's College London
      • • Department of Psychological Medicine
      • • Institute of Psychiatry
      Londinium, England, United Kingdom
  • 2013
    • University of Nottingham
      • Institute of Mental Health
      Nottingham, ENG, United Kingdom
    • ICL
      Londinium, England, United Kingdom
    • Università degli Studi di Modena e Reggio Emilia
      • Department of Life Sciences
      Modena, Emilia-Romagna, Italy
  • 2012
    • University College London
      • Department of Epidemiology and Public Health
      London, ENG, United Kingdom
    • Università degli Studi di Brescia
      • Department of Clinical and Experimental Sciences
      Brescia, Lombardy, Italy
  • 2008–2009
    • The Kings College
      Johnson Lane, Nevada, United States
    • The University of Edinburgh
      • Queen's Medical Research Institute
      Edinburgh, SCT, United Kingdom
    • Taipei Medical University
      • Graduate Institute of Nutrition and Health Sciences
      T’ai-pei, Taipei, Taiwan
  • 2006–2008
    • China Medical University Hospital
      • Department of Psychiatry
      臺中市, Taiwan, Taiwan
  • 1994–2005
    • Università degli studi di Cagliari
      • Department of Public Health, Clinical and Molecular Medicine
      Cagliari, Sardinia, Italy
  • 2004
    • University of London
      Londinium, England, United Kingdom
  • 1995–1998
    • Emory University
      • Department of Psychiatry and Behavioral Sciences
      Atlanta, GA, United States