Announcement of Retraction

The editorial board announced this article has been retracted on July 6, 2022. If you have any further question, please contact us at: [email protected]

Preserved subliminal processing and impaired conscious access in schizophrenia.

BACKGROUND: Studies of visual backward masking have frequently revealed an elevated masking threshold in schizophrenia. This finding has frequently been interpreted as indicating a low-level visual deficit. However, more recent models suggest that masking may also involve late and higher-level integrative processes, while leaving intact early bottom-up visual processing. OBJECTIVE: To test the hypothesis that the backward-masking deficit in schizophrenia corresponds to a deficit in the late stages of conscious perception, whereas the subliminal processing of masked stimuli is fully preserved. DESIGN: Twenty-eight patients with schizophrenia and 28 normal control subjects performed 2 backward-masking experiments. We used Arabic digits as stimuli and varied quasi-continuously the interval with a subsequent mask, thus allowing us to progressively unmask the stimuli. We finely quantified their degree of visibility using objective and subjective measures to evaluate the threshold duration for access to consciousness. We also studied the priming effect caused by the variably masked numbers in a comparison task performed on a subsequently presented and highly visible target number. RESULTS: The threshold delay between the digit and mask necessary for the conscious perception of the masked stimulus was longer in patients compared with controls. This higher consciousness threshold in patients was confirmed by an objective and a subjective measure, and both measures were highly correlated for the patients and controls. However, subliminal priming of masked numbers was effective and identical in patients and controls. CONCLUSIONS: Access to conscious report of masked stimuli is impaired in schizophrenia, whereas fast bottom-up processing of the same stimuli, as assessed by subliminal priming, is preserved. These findings suggest a high-level origin of the masking deficit in schizophrenia, although they leave open for further research its exact relation to previously identified bottom-up visual processing abnormalities

Contribution au demembrement phenotypique et a la validation nosologique des conduites suicidaires

Ce travail s articule autour du constat de l hétérogénéité phénotypique des conduitessuicidaires conjointement à celui de l existence de nombreux facteurs de validité nosologique.En suivant la méthode du symptôme candidat, nous avons pu montrer que la distribution del âge à la première tentative de suicide (TS) était une mixture de deux distributionsgaussiennes. Ce symptôme candidat nous a permis de délimiter deux sous groupes distincts depatients en terme de caractéristiques cliniques. Parallèlement, l exploration des dysfonctionscognitives de patients suicidants nous a permis de proposer un deuxième symptôme candidat :le déficit de l inhibition cognitive. Enfin, grâce à l analyse en composante principale d uninstrument de mesure de la léthalité suicidaire, nous avons pu montrer que la sous dimensionde léthalité implémentation du patient constituait un symptôme candidat du fait de sesliens probables avec l intentionnalité suicidaire, deux dimensions intriquées et déterminantesdans la genèse de conduites suicidaires. Notre contribution a la validation nosologique desconduites suicidaires concerne les résultats obtenus à partir de l étude d une population depatients bipolaires au sein de laquelle l héritabilité des conduites suicidaires est apparuindépendante de celle du trouble bipolaire de l humeur. Enfin, au sein d une populationépidémiologique psychiatrique martiniquaise homogène sur le plan ethnique, 18% despatients avaient des antécédents de TS. Ce chiffre est inférieur à celui mesuré au sein d étudesmenées en population cliniques majoritairement caucasiennes et conforte l idée d une hyposuicidalité dans les populations d origine africaine.This work starts with the report of the phenotypic heterogeneity of suicidal behavior jointly tothat of the existence of several nosological validity factors. While following the candidatesymptom approach, we could show that the distribution of the age at first suicide attempt(SA) was a mixture of two Gaussian distributions. This candidate symptom enabled us todelimit two distinct groups of patients in term of clinical characteristics. In parallel, theexploration of the cognitive dysfunctions among suicidal patients enabled us to propose asecond candidate symptom: the impaired cognitive inhibition. Lastly, by the study of asuicidal lethality scale, we could show that the patient s implementation represented acandidate symptom because of its probable relationship with suicidal intent, two intricate anddetermining dimensions in the genesis of suicidal behavior. Our contribution to thenosological validation of suicidal behavior relates to the results obtained from the study of apopulation of bipolar patients within whom the heritability of suicidal behavior appearedindependent of that of the bipolar disorder. Lastly, among an Afro-Caribbeanepidemiological psychiatric sample, 18% of the patients had a history of SA. This rate islower than that measured within studies conducted among mainly Caucasian clinical samplesand strengthen the idea of a hypo-suicidality in the populations of African origin.PARIS-EST-Université (770839901) / SudocPARIS12-Bib. électronique (940280011) / SudocSudocFranceF

Brain Versus Blood: A Systematic Review on the Concordance Between Peripheral and Central Kynurenine Pathway Measures in Psychiatric Disorders

Objective: Disturbances in the kynurenine pathway have been implicated in the pathophysiology of psychotic and mood disorders, as well as several other psychiatric illnesses. It remains uncertain however to what extent metabolite levels detectable in plasma or serum reflect brain kynurenine metabolism and other disease-specific pathophysiological changes. The primary objective of this systematic review was to investigate the concordance between peripheral and central (CSF or brain tissue) kynurenine metabolites. As secondary aims we describe their correlation with illness course, treatment response, and neuroanatomical abnormalities in psychiatric diseases. Methods: We performed a systematic literature search until February 2021 in PubMed. We included 27 original research articles describing a correlation between peripheral and central kynurenine metabolite measures in preclinical studies and human samples from patients suffering from neuropsychiatric disorders and other conditions. We also included 32 articles reporting associations between peripheral KP markers and symptom severity, CNS pathology or treatment response in schizophrenia, bipolar disorder or major depressive disorder. Results: For kynurenine and 3-hydroxykynurenine, moderate to strong concordance was found between peripheral and central concentrations not only in psychiatric disorders, but also in other (patho)physiological conditions. Despite discordant findings for other metabolites (mainly tryptophan and kynurenic acid), blood metabolite levels were associated with clinical symptoms and treatment response in psychiatric patients, as well as with observed neuroanatomical abnormalities and glial activity. Conclusion: Only kynurenine and 3-hydroxykynurenine demonstrated a consistent and reliable concordance between peripheral and central measures. Evidence from psychiatric studies on kynurenine pathway concordance is scarce, and more research is needed to determine the validity of peripheral kynurenine metabolite assessment as proxy markers for CNS processes. Peripheral kynurenine and 3-hydroxykynurenine may nonetheless represent valuable predictive and prognostic biomarker candidates for psychiatric disorders

Association between the PPP3CC gene, coding for the calcineurin gamma catalytic subunit, and bipolar disorder

<p>Abstract</p> <p>Background</p> <p>Calcineurin is a neuron-enriched phosphatase that regulates synaptic plasticity and neuronal adaptation. Activation of calcineurin, overall, antagonizes the effects of the cyclic AMP activated protein/kinase A. Thus, kinase/phosphatase dynamic balance seems to be critical for transition to long-term cellular responses in neurons, and disruption of this equilibrium should induce behavioral impairments in animal models. Genetic animal models, as well as post-mortem studies in humans have implicated calcineurin dependent calcium and cyclic AMP regulated phosphorylation/dephosphorylation in both affective responses and psychosis. Recently, genetic association between schizophrenia and genetic variation of the human calcineurin A gamma subunit gene (PPP3CC) has been reported.</p> <p>Methods</p> <p>Based on the assumption of the common underlying genetic factor in schizophrenia and bipolar affective disorder (BPAD), we performed association analysis of CC33 and CCS3 polymorphisms of the PPP3CC gene reported to be associated with schizophrenia in a French sample of 115 BPAD patients and 97 healthy controls.</p> <p>Results</p> <p>Carrying 'CT' or 'TT' genotypes of the PPP3CC-CC33 polymorphism increased risk to develop BPAD comparing to carry 'CC' genotype (OR = 1.8 [1.01–3.0]; p = 0.05). For the PPP3CC-CCS3 polymorphism, 'AG' or 'GG' carriers have an increased risk to develop BPAD than 'AA' carriers (OR = 2.8 [1.5–5.2]). The CC33 and CCS3 polymorphisms were observed in significant linkage disequilibrium (D' = 0.91, r²= 0.72). Haplotype frequencies were significantly different in BPAD patients than in controls (p = 0.03), with a significant over-transmission of the 'TG' haplotype in BPAD patients (p = 0.001).</p> <p><b>Conclusion:</b></p> <p>We suggest that the PPP3CC gene might be a susceptibility gene for BPAD, in accordance with current neurobiological hypotheses that implicate dysregulation of signal-transduction pathways, such as those regulated by calcineurin, in the etiology of affective disorders.</p