Publications by authors named "Anne-Cecile Petit"

In most mammals, new neurons are not only produced during embryogenesis but also after birth. Soon after adult neurogenesis was discovered, the influence of recruiting new neurons on cognitive functions, especially on memory, was documented. Likewise, the late process of neuronal production also contributes to affective functions, but this outcome was recognized with more difficulty.

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Article Synopsis
  • Esketamine has been proven effective for treatment-resistant depression (TRD), but its high cost and limited knowledge on treatment duration highlight the need for better outcome predictions.* -
  • A study with TRD patients receiving esketamine identified two response trajectories—responders and non-responders—while showing that initial depression scores can predict future treatment success with 80% accuracy.* -
  • Although the findings are promising, the study's observational nature and lack of a placebo group mean more controlled experiments are needed to validate these predictions and improve treatment decisions.*
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Introduction: Urgent action is needed to fight the ongoing coronavirus disease 2019 (COVID-19) pandemic by reducing the number of infected cases, contagiousness and severity. Chlorpromazine (CPZ), an antipsychotic from the phenothiazine group, is known to inhibit clathrin-mediated endocytosis and has antiviral activity against severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1) and Middle East respiratory syndrome coronavirus. The aim of this in-vitro study was to test CPZ against SARS-CoV-2 in monkey and human cells.

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Since the 1950s, the therapeutic arsenal against depression has grown considerably. From the discovery of mono-amine oxidase inhibitors (MAOIs) to the antidepressant effect of ketamine, several pharmacological breakthroughs made the history of psychiatry. These discoveries oriented the research about the pathophysiology of depression, which is one of the most disabling diseases worldwide affecting 10 to 20% of general population.

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Major depressive disorder is a complex multifactorial condition with a so far poorly characterized underlying pathophysiology. Consequently, the available treatments are far from satisfactory as it is estimated that up to 30% of patients are resistant to conventional treatment. Recent comprehensive evidence has been accumulated which suggests that inflammation may be implied in the etiology of this disease.

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The study of genetic polymorphisms involved in antidepressants (AD) response is essential to provide a personalized medicine approach in the field of depression. β-arrestin 2 (ARRB2) is a candidate gene in the pharmacogenetics of AD as it is involved in the signaling cascade downstream of numerous neurotransmitter receptors. We investigated the association between five ARRB2 single nucleotide polymorphisms (SNPs): rs1045280, rs2036657, rs4790694, rs3786047 and rs452246, and response to AD treatment in a sample of 569 patients with a major depressive episode treated for 6months.

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Aim: NTRK2 is the main receptor of the brain derived neurotrophic factor, which is involved in antidepressant efficacy. We assessed the impact of eight NTRK2 SNPs pertaining to response and remission after antidepressant treatment in depressed patients.

Patients & Methods: In a naturalistic study, 569 patients with a major depressive episode requiring a new antidepressant treatment were genotyped for eight NTRK2 SNPs (rs1187352, rs1439050, rs1778933 rs2289656, rs2289657, rs2289658, rs3824519, rs56142442) and prospectively assessed for response and remission after 6 months of treatment.

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Objectives: Very preterm infants are known to be at risk of developmental disabilities and behavioural disorders. This condition is supposed to alter mother-infant interactions. Here we hypothesize that the parental coping with the very preterm birth may greatly influence mother-infant interactions.

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Article Synopsis
  • Pharmacological studies reveal that the serotonin 2A (5-HT2A) receptor may play a significant role in how patients with major depressive disorder (MDD) respond to antidepressant drugs (ADs), but the influence of genetic variations in the HTR2A gene on treatment outcomes is still unclear.
  • A study involving both depressed patients and genetically modified mice focused on specific single nucleotide polymorphisms (SNPs) in the HTR2A gene to assess their impact on antidepressant responses, finding that certain genetic profiles were associated with poorer treatment outcomes.
  • Results suggest that the 5-HT2A receptor is crucial in mediating the effects of chronic SSRI treatment, as its absence diminished the efficacy
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Background: Whether the Brain Derived Neurotrophic Factor (BDNF) Val66Met polymorphism can predict antidepressant drug efficacy in depressed patients remains unclear, suggesting that it may depend on antidepressant classes. We assessed the impact of Val66Met polymorphism on antidepressant response and remission depending on antidepressant classes.

Methods: In a 6-month prospective, real-world setting, treatment study, 345 Caucasian depressed patients requiring a new or different drug treatment with a selective serotonin reuptake inhibitor (SSRI), a serotonin and noradrenalin reuptake inhibitor (SNRI) or a tricyclic antidepressant (TCA), were genotyped and assessed for response and remission.

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An association between serotonin 2A receptor (5-HT2AR), encoded by HTR2A gene, and major depressive disorder (MDD) has been suggested. Here, we combined preclinical and ecological clinical approaches to explore the impact of impaired 5-HT2AR-mediated transmission on MDD or anxio-depressive-like phenotype in mice. Htr2a knock-out mice (Htr2a(-/-)) and wild-type mice were compared for the ability of chronic corticosterone to elicit some anxio-depressive-like phenotype in three behavioral paradigms (elevated plus maze, tail suspension test and splash test).

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To study the cell behavior during morphogenesis of mouse surface ectoderm, skin, and hair follicles, we (1-3) have developed a new method to temporally induce clones that is based on a tamoxifen-dependent Cre recombinase. The classical protocol consisting in dissolving 4-hydroxy-tamoxifen or tamoxifen in corn oil to perform intraperitoneal (ip) injections (4) is not optimal to control the pharmacokinetic parameters of the induction as it leads to experimental variability in terms of timing and level of induction. We have developed a new protocol that consists in solubilizing 4-OHT or tamoxifen in an aqueous solvent using Cremophor(®) EL (5).

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Background: Understanding the series of morphogenetic processes that underlie the making of embryo structures is a highly topical issue in developmental biology, essential for interpreting the massive molecular data currently available. In mouse embryo, long-term in vivo analysis of cell behaviours and movements is difficult because of the development in utero and the impossibility of long-term culture.

Methodology/principal Findings: We improved and combined two genetic methods of clonal analysis that together make practicable large-scale production of labelled clones.

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During development, embryonic cells display a large variety of behaviors that lead to the formation of embryonic structures that are frequently transient. Simultaneously, cells progress towards a specific fate. The current challenge for embryologists is to resolve how these two distinct aspects of development co-exist.

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Segmentation of the vertebrate body axis is initiated early in development with the sequential formation of somites. Somitogenesis is temporally regulated by a molecular oscillator, the segmentation clock, which acts within presomitic mesoderm (PSM) cells to drive periodic expression of the cyclic genes. We have investigated the kinetics of the progression of cycling gene expression along the PSM.

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