Journal of psychiatry & neuroscience: JPN (J Psychiatr Neurosci)

Description

The Journal of Psychiatry & Neuroscience publishes original research articles and review papers in clinical psychiatry (adult and child) and neuroscience that relate to major psychiatric disorders, particularly schizophrenia, affective disorders and neurodegenerative diseases. The journal therefore provides a forum for original basic and clinical science research that will present its readership with an integrated perspective on current and emerging issues in clinical and biological psychiatry. In this respect, the Journal of Psychiatry & Neuroscience represents a new and unique concept in communication that will bring together the latest advances in both psychiatry and neuroscience.

Publications in this journal

• Psychiatry's age of enlightenment: optogenetics and the discovery of novel targets for the treatment of psychiatric disorders

  Authors: Michelle M Sidor

  Journal of psychiatry & neuroscience : JPN. 01/2012; 37(1):4-6.

• Adverse events associated with switching antipsychotics

  Authors: Johnny Su, Alasdair M Barr, Ric M Procyshyn

  Journal of psychiatry & neuroscience : JPN. 01/2012; 37(1):E1-2.

• Discontinuation of lithium because of side effects

  Authors: Tomas Hajek, Martin Alda, Paul Grof

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):E39-40.

• Event-related potentials and changes of brain rhythm oscillations during working memory activation in patients with first-episode psychosis

  Authors: Pascal Missonnier, François R Herrmann, Adriano Zanello, Maryse Badan Bâ, Logos Curtis, Diana Canovas, Fabrice Chantraine, Jonas Richiardi, Panteleimon Giannakopoulos, Marco C G Merlo

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110033.

  Background: Earlier contributions have documented significant changes in sensory, attention-related endogenous event-related potential (ERP) components and θ band oscillatory responses during workingBackground: Earlier contributions have documented significant changes in sensory, attention-related endogenous event-related potential (ERP) components and θ band oscillatory responses during working memory activation in patients with schizophrenia. In patients with first-episode psychosis, such studies are still scarce and mostly focused on auditory sensory processing. The present study aimed to explore whether subtle deficits of cortical activation are present in these patients before the decline of working memory performance. Methods: We assessed exogenous and endogenous ERPs and frontal θ event-related synchronization (ERS) in patients with first-episode psychosis and healthy controls who successfully performed an adapted 2-back working memory task, including 2 visual n-back working memory tasks as well as oddball detection and passive fixation tasks. Results: We included 15 patients with first-episode psychosis and 18 controls in this study. Compared with controls, patients with first-episode psychosis displayed increased latencies of early visual ERPs and phasic θ ERS culmination peak in all conditions. However, they also showed a rapid recruitment of working memory-related neural generators, even in pure attention tasks, as indicated by the decreased N200 latency and increased amplitude of sustained θ ERS in detection compared with controls. Limitations: Owing to the limited sample size, no distinction was made between patients with first-episode psychosis with positive and negative symptoms. Although we controlled for the global load of neuroleptics, medication effect cannot be totally ruled out. Conclusion: The present findings support the concept of a blunted electroencephalographic response in patients with first-episode psychosis who recruit the maximum neural generators in simple attention conditions without being able to modulate their brain activation with increased complexity of working memory tasks.

• Voxel-wise meta-analysis of fMRI studies in patients at clinical high risk for psychosis

  Authors: Paolo Fusar-Poli

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110021.

  Background: Reliable neurofunctional markers of increased vulnerability to psychosis are needed to improve the predictive value of psychosis risk syndrome and inform preventive interventions.Background: Reliable neurofunctional markers of increased vulnerability to psychosis are needed to improve the predictive value of psychosis risk syndrome and inform preventive interventions. Methods: I performed a signed differential mapping (SDM) voxel-wise meta-analysis of functional magnetic resonance imaging (fMRI) studies of patients at clinical high risk for psychosis. Results: Ten studies were included in the analysis. Compared with controls, high-risk patients showed reduced neural activation in the left inferior frontal gyrus (Brodmann area [BA] 9) and in a cluster spanning the bilateral medial frontal gyrus (BA8,6), bilateral superior frontal gyrus (BA8,6) and the left anterior cingulate (BA32). There was no publication bias. Heterogeneity across studies was low. Sensitivity analysis confirmed the robustness of the findings. Limitations: The cross-sectional nature of the included studies prevented the comparison of high-risk patients who later experienced a psychotic episode with those who did not. Other caveats are reflected in methodologic heterogeneity across tasks employed by different individual imaging studies. Conclusion: Reduced neurofunctional activation in prefrontal regions may represent a neurophysiologic correlate of increased vulnerability to psychosis.

• Stress response in postpartum women with and without obsessive-compulsive symptoms: an fMRI study

  Authors: Catherine Lord, Meir Steiner, Claudio N Soares, Caitlin L Carew, Geoffrey B Hall

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110005.

  Background: During the postpartum period, some women might be under a considerable amount of stress and at increased risk for onset or exacerbation of obsessive-compulsive disorder (OCD). Little isBackground: During the postpartum period, some women might be under a considerable amount of stress and at increased risk for onset or exacerbation of obsessive-compulsive disorder (OCD). Little is known about the stress response correlates during the postpartum period and in patients with OCD. This study aimed to examine the cerebral, psychologic and endocrine correlates of the stress response in patients with OCD and during the postpartum period. Methods: Women with postpartum OCD, healthy postpartum women and healthy mothers past the postpartum period underwent functional magnetic resonance imaging while facing a reliable psychosocial stressor (the Montreal Imaging Stress Task). Stress-related psychologic and endocrine responses (i.e., cortisol) were obtained. Results: We enrolled 12 women with postpartum OCD, 16 healthy postpartum women and 11 healthy mothers past the postpartum period in our study. Compared with healthy postpartum counterparts, postpartum women with OCD had a heightened self-reported and endocrine stress response associated with a distinct brain activation pattern in response to psychosocial stress involving the orbitofrontal and temporal cortices. Moreover, compared with mothers assessed in a period of time beyond the postpartum period, healthy postpartum women did not differ in psychologic and cortisol response to stress, but recruited different brain regions, such as the dorsolateral prefrontal cortex and the anterior cingulate cortex, during exposure to stress. Limitations: Potential confounding factors, such as medication use, breastfeeding, parity and personality factors, may have modulated the stress-related endocrine response and could not be assessed in this study. Conclusion: Obsessive-compulsive disorder and the postpartum period differentially influence the brain circuitry underlying psychosocial stress as well as the psychologic and endocrine responses.

• What is a functional genetic polymorphism? Defining classes of functionality

  Authors: Paul R Albert

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):363-5.

• Effects of early-life adversity on white matter diffusivity changes in patients at risk for major depression

  Authors: Thomas Frodl, Angela Carballedo, Andrew J Fagan, Danuta Lisiecka, Yolande Ferguson, James F Meaney

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110028.

  Background: Relatives of patients with major depressive disorder (MDD) and people who experienced early-life adversity are at risk for MDD. The aim of our study was to investigate whether unaffectedBackground: Relatives of patients with major depressive disorder (MDD) and people who experienced early-life adversity are at risk for MDD. The aim of our study was to investigate whether unaffected first-degree healthy relatives (UHRs) of patients with MDD show changes in white matter fibre connections compared with healthy controls and whether there are interactions between early-life adversity and these microstructural changes. Methods: Unaffected, healthy first-degree relatives of patients with MDD and healthy controls without any family history for a psychiatric disease underwent high angular resolution diffusion imaging with 61 diffusion directions. Data were analyzed with tract-based spatial statistics, and findings were confirmed with tractography. Results: Twenty-one UHRs and 24 controls participated in our study. The UHRs showed greater fractional anisotropy than controls in the body and splenium of the corpus callosum, inferior fronto-occipital fasciculus (IFO), left superior longitudinal fasciculus (SLF) and right fornix. The UHRs who experienced more early-life adversity had greater fractional anisotropy than those with less early-life adversity in the splenium of the corpus callosum, fornix, IFO and SLF; in controls, early-life adversity was found to be associated with decreased fractional anisotropy in these fibre tracts. Limitations: Studying participants' strategies for coping with early-life adversity would have been helpful. Crossing fibres intracts are a general limitation of the method used. Conclusion: Altogether, our findings provide evidence for greater fractional anisotropy in UHRs and for interaction between early-life adversity and family risk on white matter tracts involved in cognitive-emotional processes. Whether stronger neural fibre connections are associated with more resilience against depression needs to be addressed in future studies.

• Long-term administration of the dopamine D3/2 receptor agonist pramipexole increases dopamine and serotonin neurotransmission in the male rat forebrain

  Authors: Olga Chernoloz, Mostafa El Mansari, Pierre Blier

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110038.

  Background: Long-term administration of the dopamine (DA) D2-like (D3/2) receptor agonist pramipexole (PPX) has been previously found to desensitize D2 autoreceptors, thereby allowing a normalizationBackground: Long-term administration of the dopamine (DA) D2-like (D3/2) receptor agonist pramipexole (PPX) has been previously found to desensitize D2 autoreceptors, thereby allowing a normalization of the firing of DA neurons and serotonin (5-HT)(1A) autoreceptors, permitting an enhancement of the spontaneous firing of 5-HT neurons. We hypothesized that PPX would increase overall DA and 5-HT neurotransmission in the forebrain as a result of these changes at the presynaptic level. Methods: Osmotic minipumps were implanted subcutaneously in male Sprague-Dawley rats, delivering PPX at a dose of 1 mg/kg/d for 14 days. The in vivo electrophysiologic microiontophoretic experiments were carried out in anesthetized rats. Results: The sensitivity of postsynaptic D2 receptors in the prefrontal cortex (PFC) remained unaltered following PPX administration, as indicated by the unchanged responsiveness to the microiontophoretic application of DA. Their tonic activation was, however, significantly increased by 104% compared with the control level. The sensitivity of postsynaptic 5-HT(1A) receptors was not altered, as indicated by the unchanged responsiveness to the microiontophoretic application of 5-HT. Similar to other antidepressant treatments, long-term PPX administration enhanced the tonic activation of 5-HT(1A) receptors on CA3 pyramidal neurons by 142% compared with the control level. Limitations: The assessment of DA and 5-HT neuronal tone was restricted to the PFC and the hippocampus, respectively. Conclusion: Chronic PPX administration led to a net enhancement in DA and 5-HT neuro transmission, as indicated by the increased tonic activation of postsynaptic D2 and 5-HT(1A) receptors in forebrain structures.

• Is the Gly82Ser polymorphism in the RAGE gene relevant to schizophrenia and the personality trait psychoticism?

  Authors: Petra Suchankova, Jonas Klang, Carin Cavanna, Göran Holm, Staffan Nilsson, Erik G Jönsson, Agneta Ekman

  Journal of psychiatry & neuroscience : JPN. 11/2011; 36(6):110024.

  Background: The receptor for advanced glycation end products (RAGE) is the main receptor for S100B, an astrogial proinflammatory mediator that has been suggested to be involved in the pathophysiologyBackground: The receptor for advanced glycation end products (RAGE) is the main receptor for S100B, an astrogial proinflammatory mediator that has been suggested to be involved in the pathophysiology of schizophrenia. To further elucidate the possible relevance of inflammation for mental functions, we investigated a functional polymorphism in the gene coding for RAGE in relation to personality traits and susceptibility to schizophrenia. Methods: We studied the Gly82Ser polymorphism (rs2070600, 244G>A) in 2 population-based cohorts of middle-aged participants assessed using the Karolinska Scales of Personality. In addition, we compared genotype frequencies between patients with schizophrenia and controls. Results: The population-based cohorts included 270 women and 247 men, and the case-control study involved 138 patients with schizophrenia and 258 controls. In the population-based cohorts, 82Ser carriers were found to have significantly higher scores for the psychoticism personality trait comprising the detachment and suspicion subscales. The case-control study revealed that the 82Ser allele was significantly more frequent among patients than controls. Limitations: This study was limited by the modest sample size and the use of a self-report measure to assess personality traits. Conclusion: Our findings suggest that the proven relation between certain personality traits and schizophrenia can at least to some extent be explained on a genetic level. Also, the activated S100B-RAGE axis may be an underlying cause, not only a consequence, of the disease.

• Bright light for nonseasonal depression?

  Authors: Simon N Young

  Journal of psychiatry & neuroscience : JPN. 09/2011; 36(5):E37-8.

• Working memory processing of traumatic material in women with posttraumatic stress disorder

  Authors: Lionel Landré, Christophe Destrieux, Frédéric Andersson, Laurent Barantin, Yann Quidé, Géraldine Tapia, Nematollah Jaafari, David Clarys, Philippe Gaillard, Michel Isingrini, Wissam El-Hage

  Journal of psychiatry & neuroscience : JPN. 09/2011; 36(5):100167.

  Background: Posttraumatic stress disorder (PTSD) is associated with medial frontal and amygdala functional alterations during the processing of traumatic material and frontoparietal dysfunctionsBackground: Posttraumatic stress disorder (PTSD) is associated with medial frontal and amygdala functional alterations during the processing of traumatic material and frontoparietal dysfunctions during working memory tasks. This functional magnetic resonance imaging (fMRI) study investigated the effects of trauma-related words processing on working memory in patients with PTSD. Methods: We obtained fMRI scans during a 3-back task and an identity task on both neutral and trauma-related words in women with PTSD who had been sexually abused and in healthy, nonexposed pair-matched controls. Results: Seventeen women with PTSD and 17 controls participated in the study. We found no behavioural working memory deficit for the PTSD group. In both tasks, deactivation of posterior parietal midline regions was more pronounced in patients than controls. Additionally, patients with PTSD recruited the left dorsolateral frontal sites to a greater extent during the processing of trauma-related material than neutral material. Limitations: This study included only women and did not include a trauma-exposed non-PTSD control group; the results may, therefore, have been influenced by sex or by effects specific to trauma exposure. Conclusion: Our results broadly confirm frontal and parietal functional variations in women with PTSD and suggest a compensatory nature of these variations with regard to the retreival of traumatic memories and global attentional deficits, respectively, during cognitively challenging tasks.

• Inflaming depression

  Authors: Hymie Anisman

  Journal of psychiatry & neuroscience : JPN. 09/2011; 36(5):291-5.

• My 21 years with the Journal of Psychiatry and Neuroscience, with observations on editors, editorial boards, authors and reviewers

  Authors: Simon N Young

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):E30-4.

• Kynurenine 3-monooxygenase polymorphisms: relevance for kynurenic acid synthesis in patients with schizophrenia and healthy controls

  Authors: Maria Holtze, Peter Saetre, Göran Engberg, Lilly Schwieler, Thomas Werge, Ole A Andreassen, Håkan Hall, Lars Terenius, Ingrid Agartz, Erik G Jönsson, Martin Schalling, Sophie Erhardt

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):100175.

  Background: Patients with schizophrenia show increased brain and cerebrospinal fluid (CSF) concentrations of the endogenous N-methyl-D-aspartate receptor antagonist kynurenic acid (KYNA). ThisBackground: Patients with schizophrenia show increased brain and cerebrospinal fluid (CSF) concentrations of the endogenous N-methyl-D-aspartate receptor antagonist kynurenic acid (KYNA). This compound is an end-metabolite of the kynurenine pathway, and its formation indirectly depends on the activity of kynurenine 3-monooxygenase (KMO), the enzyme converting kynurenine to 3-hydroxykynurenine. Methods: We analyzed the association between KMO gene polymorphisms and CSF concentrations of KYNA in patients with schizophrenia and healthy controls. Fifteen single nucleotide polymorphisms (SNPs) were selected covering KMO and were analyzed in UNPHASED. Results: We included 17 patients with schizophrenia and 33 controls in our study. We found an association between a KMO SNP (rs1053230), encoding an amino acid change of potential importance for substrate interaction, and CSF concentrations of KYNA. Limitations: Given the limited sample size, the results are tentative until replication. Conclusion: Our results suggest that the nonsynonymous KMO SNP rs1053230 influences CSF concentrations of KYNA.

• Abnormal hippocampal activation in patients with extensive history of major depression: an fMRI study

  Authors: Andrea M B Milne, Glenda M Macqueen, Geoffrey B C Hall

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):110004.

  Background: Impairment of recollection memory is consistently reported in patients with major depressive disorder (MDD) and may reflect underlying functional hippocampal changes, particularly inBackground: Impairment of recollection memory is consistently reported in patients with major depressive disorder (MDD) and may reflect underlying functional hippocampal changes, particularly in those with extensive histories of illness. We hypothesized that relative to controls, patients with a protracted course of illness would show diminished hippocampal activation on functional magnetic resonance imaging (fMRI) during a recollection memory task. Methods: Patients who experienced 3 or more previously treated depressive episodes were compared with age- and sex-matched controls. We acquired fMRI data while participants performed a recollection memory process dissociation task. Results: Using bilateral regions of interest (ROIs) prescribed for the right and left hippocampal/parahippocampal complex, we observed increased activation of the right hippocampal and left parahippocampal gyrus in controls compared with patients with MDD during recollection memory trials. Within-group comparisons revealed heightened engagement of the hippocampal head (R/L) for controls during recollection trials, and greater activation of the hippocampal body/tail (R/L) during the learn-list encoding period in both the MDD and control groups. Recollection memory performance was significantly correlated with changes in blood oxygen level-dependent signal during recollection trials in the ROIs of the right hippocampus and right hippocampal head. Limitations: This study was limited by the inclusion of patients taking antidepressant medication, raising the possibility that the reported findings were treatment effects. Conclusion: The findings of decreased recruitment of the right hippocampal and left parahippocampal gyrus in patients with MDD suggest that these regions may be sensitive to the impact of disease burden and repeated episodes of MDD. This attenuated activation may represent stable changes in hippocampal function that occur over the course of illness in patients with MDD. The findings from within-group comparisons show that the group differences in the activation of the right hippocampal head were driven by greater engagement of this region among controls during recollection memory performance. These results also associate recollection performance impairments in patients with MDD with diminished hippocampal engagement.

• A role for Akt and glycogen synthase kinase-3 as integrators of dopamine and serotonin neurotransmission in mental health

  Authors: Jean-Martin Beaulieu

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):110011.

  Mental illnesses, such as bipolar disorder, attention-deficit/hyperactivity disorder, depression and schizophrenia are a major public health concern worldwide. Several pharmacologic agents acting onMental illnesses, such as bipolar disorder, attention-deficit/hyperactivity disorder, depression and schizophrenia are a major public health concern worldwide. Several pharmacologic agents acting on monoamine neurotransmission are used for the management of these disorders. However, there is still little understanding of the ultimate molecular mechanisms responsible for the therapeutic effects of these drugs or their relations with disease etiology. Here I provide an overview of recent advances on the involvement of the signalling molec ules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behaviour by the monoamine neurotransmitters dopamine (DA) and serotonin (5-HT). I examine the possible participation of these signalling molecules to the effects of antidepressants, lithium and antipsychotics, as well as their possible contribution to mental disorders. Regulation of Akt and GSK3 may constitute an important signalling hub in the subcellular integration of 5-HT and DA neurotransmission. It may also provide a link between the action of these neurotransmitters and gene products, like disrupted in schizophrenia 1 (DISC1) and neuregulin (NRG), that are associated with increased risk for mental disorders. However, changes in Akt and GSK3 signalling are not restricted to a single disorder, and their contribution to specific behavioural symptoms or therapeutic effects may be modulated by broader changes in biologic contexts or signalling landscapes. Under standing these interactions may provide a better understanding of mental illnesses, leading to better efficacy of new therapeutic approaches.

• Dysconnectivity of multiple resting-state networks in patients with schizophrenia who have persistent auditory verbal hallucinations

  Authors: Nadine Donata Wolf, Fabio Sambataro, Nenad Vasic, Karel Frasch, Markus Schmid, Carlos Schönfeldt-Lecuona, Philipp Arthur Thomann, Robert Christian Wolf

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):110008.

  Background: Functional neuroimaging studies on schizophrenia have suggested abnormal task-related functional connectivity in patients with schizophrenia who have auditory verbal hallucinationsBackground: Functional neuroimaging studies on schizophrenia have suggested abnormal task-related functional connectivity in patients with schizophrenia who have auditory verbal hallucinations (AVHs). However, little is known about intrinsic functional connectivity in these patients. Methods: Between January 2009 and February 2010, we studied patients with schizophrenia who had persistent and treatment-refractory AVHs in comparison with healthy controls. Using functional magnetic resonance imaging, we studied the functional connectivity of multiple resting state networks (RSNs) and their relation to symptom severity. We analyzed the data using a spatial group independent component analysis, and we used random-effects t tests to compare spatial components between groups. Results: There were 10 patients and 14 controls enrolled in this study. In total, 16 RSNs were identified, from which we selected 4 networks of interest for further analyses. Within a speech-related network, patients showed increased connectivity in bilateral temporal regions and decreased connectivity in the cingulate cortex. Within 2 additional RSNs associated with attention and executive control, respectively, patients exhibited abnormal connectivity in the precuneus and right lateral prefrontal areas. We found correlations between measures of AVH severity and functional connectivity of the left anterior cingulate, left superior temporal gyrus and right lateral prefrontal cortex. Limitations: The relatively small sample size, the patients' use of antipsychotic medication and the lack of a clinical control group have to be considered as potential limitations. Conclusion: Our findings indicate that disrupted intrinsic connectivity of a speech-related network could underlie persistent AVHs in patients with schizophrenia. In addition, the occurrence of hallucinatory symptoms seems to modulate RSNs associated with attention and executive control.

• Does the salience network play a cardinal role in psychosis? An emerging hypothesis of insular dysfunction

  Authors: Lena Palaniyappan, Peter F Liddle

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):100176.

  The insular cortex is one of the brain regions that show consistent abnormalities in both structural and functional neuroimaging studies of schizophrenia. In healthy individuals, the insula has beenThe insular cortex is one of the brain regions that show consistent abnormalities in both structural and functional neuroimaging studies of schizophrenia. In healthy individuals, the insula has been implicated in a myriad of physiologic functions. The anterior cingulate cortex (ACC) and insula together constitute the salience network, an intrinsic large-scale network showing strong functional connectivity. Considering the insula as a functional unit along with the ACC provides an integrated understanding of the role of the insula in information processing. In this review, we bring together evidence from imaging studies to understand the role of the salience network in schizophrenia and propose a model of insular dysfunction in psychosis.

• Managing anxiety and depressive symptoms in adults with autism-spectrum disorders

  Authors: Kerry Boyd, Marc Woodbury-Smith, Peter Szatmari

  Journal of psychiatry & neuroscience : JPN. 07/2011; 36(4):E35-6.

• Treatment of ADHD in patients unresponsive to methylphenidate

  Authors: Lily Hechtman

  Journal of psychiatry & neuroscience : JPN. 05/2011; 36(3):216.

• Parent-of-origin effects of FAS and PDLIM1 in attention-deficit/hyperactivity disorder

  Authors: Ke-Sheng Wang, Xuefeng Liu, Qunyuan Zhang, Nagesh Aragam, Yuen Pa

  Journal of psychiatry & neuroscience : JPN. 05/2011; 36(3):100173.

  Background: Previous studies have suggested that there may be a parent-of-origin effect for attention-deficit/hyperactivity disorder (ADHD) candidate genes. The objective of the present study was toBackground: Previous studies have suggested that there may be a parent-of-origin effect for attention-deficit/hyperactivity disorder (ADHD) candidate genes. The objective of the present study was to investigate parent-of-origin effects using a genome-wide association analysis of the International Multicentre ADHD Genetics (IMAGE) study sample. Methods: Family-based association analysis for ADHD using 846 ADHD probands and their parents was performed using the PLINK program, and parent-of-origin effects were studied using a Z score for the difference in paternal versus maternal odds ratios. Results: We identified 44 single nucleotide polymorphisms (SNPs) showing parent-of-origin effects at a significance level of p < 0.001. The most significant SNP, rs7614907, is at position 3q13.33 in the CDGAP gene (p = 0.000064 for parent-of-origin effect). Furthermore, 2 genes (FAS and PDLIM1) showed moderate parent-of-origin effects (p = 0.00086 for rs9658691 and p = 0.00077 for rs11188249) and strong maternal transmission (p = 0.000059 for rs9658691 and p = 0.0000068 for rs11188249). In addition, ZNF775 showed a moderate parent-of-origin effect (p = 0.00036 for rs7790549) and strong paternal transmission (p = 0.000041 for rs7790549). Limitations: We only had 1 sample available for analysis. Conclusion: These results suggest several genes or regions with moderate parent-of-origin effects, and these findings will serve as a resource for replication in other populations to elucidate the potential role of these genetic variants in ADHD.

• The 1000 Genomes Project: deep genomic sequencing waiting for deep psychiatric phenotyping

  Authors: Ridha Joober

  Journal of psychiatry & neuroscience : JPN. 05/2011; 36(3):147-9.

• Identification and management of cryptic bipolarity in patients with TRD

  Authors: Verinder Sharma

  Journal of psychiatry & neuroscience : JPN. 03/2011; 36(2):E3-4.

• N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action

  Authors: Olivia Dean, Frank Giorlando, Michael Berk

  Journal of psychiatry & neuroscience : JPN. 03/2011; 36(2):78-86.

  There is an expanding field of research investigating the benefits of alternatives to current pharmacological therapies in psychiatry. N-acetylcysteine (NAC) is emerging as a useful agent in theThere is an expanding field of research investigating the benefits of alternatives to current pharmacological therapies in psychiatry. N-acetylcysteine (NAC) is emerging as a useful agent in the treatment of psychiatric disorders. Like many therapies, the clinical origins of NAC are far removed from its current use in psychiatry. Whereas the mechanisms of NAC are only beginning to be understood, it is likely that NAC is exerting benefits beyond being a precursor to the antioxidant, glutathione, modulating glutamatergic, neurotropic and inflammatory pathways. This review outlines the current literature regarding the use of NAC in disorders including addiction, compulsive and grooming disorders, schizophrenia and bipolar disorder. N-acetylcysteine has shown promising results in populations with these disorders, including those in whom treatment efficacy has previously been limited. The therapeutic potential of this acetylated amino acid is beginning to emerge in the field of psychiatric research.

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