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Molecular Neuropsychiatry

Nathan D Okerlund, Robert E Stanley, Benjamin N R Cheyette
The transmembrane protein Vangl2, a key regulator of the Wnt/planar cell polarity (PCP) pathway, is involved in dendrite arbor elaboration, dendritic spine formation and glutamatergic synapse formation in mammalian central nervous system neurons. Cultured forebrain neurons from Vangl2 knockout mice have simpler dendrite arbors, fewer total spines, less mature spines and fewer glutamatergic synapse inputs on their dendrites than control neurons. Neurons from mice heterozygous for a semidominant Vangl2 mutation have similar but not identical phenotypes, and these phenotypes are also observed in Golgi-stained brain tissue from adult mutant mice...
July 2016: Molecular Neuropsychiatry
Joanne H Huang, Shaunna S Berkovitch, Jonathan Iaconelli, Bradley Watmuff, Hyoungjun Park, Shrikanta Chattopadhyay, Donna McPhie, Dost Öngür, Bruce M Cohen, Clary B Clish, Rakesh Karmacharya
Many studies suggest the presence of aberrations in cellular metabolism in bipolar disorder. We studied the metabolome in bipolar disorder to gain insight into cellular pathways that may be dysregulated in bipolar disorder and to discover evidence of novel biomarkers. We measured polar and nonpolar metabolites in fibroblasts from subjects with bipolar I disorder and matched healthy control subjects, under normal conditions and with two physiologic perturbations: low-glucose media and exposure to the stress-mediating hormone dexamethasone...
July 2016: Molecular Neuropsychiatry
Lindsay N Hayes, Alexey Shevelkin, Mariela Zeledon, Gary Steel, Pei-Lung Chen, Cassandra Obie, Ann Pulver, Dimitrios Avramopoulos, David Valle, Akira Sawa, Mikhail V Pletnikov
Neuregulin 3 (NRG3) is a paralog of NRG1. Genetic studies in schizophrenia demonstrate that risk variants in NRG3 are associated with cognitive and psychotic symptom severity, and several intronic single nucleotide polymorphisms in NRG3 are associated with delusions in patients with schizophrenia. In order to gain insights into the biological function of the gene, we generated a novel Nrg3 knockout (KO) mouse model and tested for neurobehavioral phenotypes relevant to psychotic disorders. KO mice displayed novelty-induced hyperactivity, impaired prepulse inhibition of the acoustic startle response, and deficient fear conditioning...
July 2016: Molecular Neuropsychiatry
Raymond R MacNeil, Daniel J Müller
The effectiveness of antipsychotic drugs is limited due to accompanying adverse effects which can pose considerable health risks and lead to patient noncompliance. Pharmacogenetics (PGx) offers a means to identify genetic biomarkers that can predict individual susceptibility to antipsychotic-induced adverse effects (AAEs), thereby improving clinical outcomes. We reviewed the literature on the PGx of common AAEs from 2010 to 2015, placing emphasis on findings that have been independently replicated and which have additionally been listed to be of interest by PGx expert panels...
July 2016: Molecular Neuropsychiatry
Christina M Hough, F Saverio Bersani, Synthia H Mellon, Elissa S Epel, Victor I Reus, Daniel Lindqvist, Jue Lin, Laura Mahan, Rebecca Rosser, Heather Burke, John Coetzee, J Craig Nelson, Elizabeth H Blackburn, Owen M Wolkowitz
Short leukocyte telomere length (LTL) may be associated with several psychiatric disorders, including major depressive disorder (MDD). Short LTL has previously been associated with poor response to psychiatric medications in bipolar disorder and schizophrenia, but no studies have prospectively assessed the relationship of LTL to SSRI response in MDD. We assessed pre-treatment LTL, depression severity (using the Hamilton Depression Rating Scale [HDRS]), and self-reported positive and negative affect in 27 healthy, unmedicated adults with MDD...
July 2016: Molecular Neuropsychiatry
Chi-Ya Kao, Zhisong He, Kathrin Henes, John M Asara, Christian Webhofer, Michaela D Filiou, Philipp Khaitovich, Carsten T Wotjak, Christoph W Turck
Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder. Several studies have attempted to characterize molecular alterations associated with PTSD, but most findings were limited to the investigation of specific cellular markers in the periphery or defined brain regions. In the current study, we aimed to unravel affected molecular pathways/mechanisms in the fear circuitry associated with PTSD. We interrogated a foot shock-induced PTSD mouse model by integrating proteomics and metabolomics profiling data...
May 2016: Molecular Neuropsychiatry
Kevin P Jensen
Substance use disorders (SUD) are a major contributor to disability and disease burden worldwide. Risk for developing SUDs is influenced by variation in the genome. Identifying the genetic variants that influence SUD risk may help us to understand the biological mechanisms for the disorders and improve treatments. Genome-wide association studies (GWAS) have been successful in identifying many regions of the genome associated with common human disorders. Here, findings from recent GWAS of SUDs that involve illicit substances will be reviewed...
May 2016: Molecular Neuropsychiatry
Meng Xia, Jantine A C Broek, Yan Jouroukhin, Jeannine Schoenfelder, Sofya Abazyan, Hanna Jaaro-Peled, Akira Sawa, Sabine Bahn, Mikhail Pletnikov
Despite the recent progress in psychiatric genetics, very few studies have focused on genetic risk factors in glial cells that, compared to neurons, can manifest different molecular pathologies underlying psychiatric disorders. In order to address this issue, we studied the effects of mutant disrupted in schizophrenia 1 (DISC1), a genetic risk factor for schizophrenia, in cultured primary neurons and astrocytes using an unbiased mass spectrometry-based proteomic approach. We found that selective expression of mutant DISC1 in neurons affects a wide variety of proteins predominantly involved in neuronal development (e...
May 2016: Molecular Neuropsychiatry
Lynn E DeLisi
The genetic mechanism for schizophrenia still remains unknown despite decades of research. A tremendous amount of investigator time and effort has gone into ascertainment of clinical samples for genetic studies over the years. Most recently, a large international effort of unprecedented collaboration has occurred to combine data worldwide in pursuit of uncovering the relevant genetic risk factors. However, in the process, the use of multiplex families to understand the genetics has waned, and it has been presumed that large resources of unrelated patients and controls are more efficient to find risk alleles than families...
May 2016: Molecular Neuropsychiatry
Trehani M Fonseka, Daniel J Müller, Sidney H Kennedy
Antipsychotic medications (APs), particularly second-generation APs, are associated with significant weight gain in schizophrenia patients. Recent evidence suggests that the immune system may contribute to antipsychotic-induced weight gain (AIWG) via AP-mediated alterations of cytokine levels. Antipsychotics with a high propensity for weight gain, such as clozapine and olanzapine, influence the expression of immune genes, and induce changes in serum cytokine levels to ultimately down-regulate neuroinflammation...
May 2016: Molecular Neuropsychiatry
(no author information available yet)
[This corrects the article DOI: 10.1159/000441252.].
May 2016: Molecular Neuropsychiatry
Stephanie Tankou, Kazuhiro Ishii, Christina Elliott, Krishna C Yalla, Jon P Day, Keiko Furukori, Ken-Ichiro Kubo, Nicholas J Brandon, Qiyi Tang, Gary Hayward, Kazunori Nakajima, Miles D Houslay, Atsushi Kamiya, George Baillie, Koko Ishizuka, Akira Sawa
DISC1 is a multifunctional, intracellular scaffold protein. At the cellular level, DISC1 plays a pivotal role in neural progenitor proliferation, migration, and synaptic maturation. Perturbation of the biological pathways involving DISC1 is known to lead to behavioral changes in rodents, which supports a clinical report of a Scottish pedigree in which the majority of family members with disruption of the DISC1 gene manifest depression, schizophrenia, and related mental conditions. The discrepancy of modest evidence in genetics but strong biological support for the role of DISC1 in mental conditions suggests a working hypothesis that regulation of DISC1 at the protein level, such as posttranslational modification, may play a role in the pathology of mental conditions...
May 2016: Molecular Neuropsychiatry
Rachel K Jonas, Maria Jalbrzikowski, Caroline A Montojo, Arati Patel, Leila Kushan, Carolyn C Chow, Therese Vesagas, Carrie E Bearden
22q11.2 deletion syndrome (22q11DS) is a neurogenetic disorder associated with elevated rates of developmental neuropsychiatric disorders and impaired executive function (EF). Disrupted brain structure-function relationships may underlie EF deficits in 22q11DS. We administered the Behavior Rating Inventory of Executive Function (BRIEF) to assess real-world EF in patients with 22q11DS and matched controls (n = 86; age 6-17 years), along with cognitive measures that tap behavioral regulation and metacognition aspects of EF...
December 2015: Molecular Neuropsychiatry
Peter M Thompson, Dianne A Cruz, Elizabeth A Fucich, Dianna Y Olukotun, Masami Takahashi, Makoto Itakura
SNAP-25 is a neurotransmitter vesicular docking protein which has been associated with brain disorders such as attention deficit hyperactivity disorder, bipolar disorder and schizophrenia. In this project, we were interested if clinical factors are associated with differential SNAP-25 expression. We examined the SNAP-25 isoform mRNA and protein levels in postmortem cortex Brodmann's area 9 (BA9) and BA24 (n = 29). Subjects were divided by psychiatric diagnosis, clinical variables including mood state in the last week of life and lifetime impulsiveness...
December 2015: Molecular Neuropsychiatry
Joseph J Shaffer, Michael J Peterson, Mary Agnes McMahon, Joshua Bizzell, Vince Calhoun, Theo G M van Erp, Judith M Ford, John Lauriello, Kelvin O Lim, Dara S Manoach, Sarah C McEwen, Daniel H Mathalon, Daniel O'Leary, Steven G Potkin, Adrian Preda, Jessica Turner, Jim Voyvodic, Cynthia G Wible, Aysenil Belger
BACKGROUND: The negative symptoms of schizophrenia include deficits in emotional expression and motivation. These deficits are stable over the course of illness and respond poorly to current medications. Previous studies have focused on negative symptoms as a single category; however, individual symptoms might be related to separate neurological disturbances. We analyzed data from the Functional Biomedical Informatics Research Network dataset to explore the relationship between individual negative symptoms and functional brain activity during an auditory oddball task...
December 2015: Molecular Neuropsychiatry
Brooke E Hjelm, Brandi Rollins, Firoza Mamdani, Julie C Lauterborn, George Kirov, Gary Lynch, Christine M Gall, Adolfo Sequeira, Marquis P Vawter
Genetic evidence has supported the hypothesis that schizophrenia (SZ) is a polygenic disorder caused by the disruption in function of several or many genes. The most common and reproducible cellular phenotype associated with SZ is a reduction in dendritic spines within the neocortex, suggesting alterations in dendritic architecture may cause aberrant cortical circuitry and SZ symptoms. Here, we review evidence supporting a multifactorial model of mitochondrial dysfunction in SZ etiology and discuss how these multiple paths to mitochondrial dysfunction may contribute to dendritic spine loss and/or underdevelopment in some SZ subjects...
December 2015: Molecular Neuropsychiatry
C Anthony Altar, Joseph Carhart, Josiah D Allen, Daniel Hall-Flavin, Joel Winner, Bryan Dechairo
DNA of 258 patients with treatment-resistant depression was collected in three 8-10 week, two-arm, prospective clinical trials. Forty-four allelic variations were measured in genes for the cytochrome P450 (CYP) enzymes CYP2D6, CYPC19, and CYP1A2, the serotonin transporter (SLC6A4), and the 5-HT2A receptor (HTR2A). The combinatorial pharmacogenomic (CPGx™) GeneSight test results were provided to clinicians to support medication changes from baseline (guided arm), or they were provided at the end of each study to clinicians of unguided patients who were treated as usual (TAU)...
October 2015: Molecular Neuropsychiatry
Mandy Johnstone, Alan Maclean, Lien Heyrman, An-Sofie Lenaerts, Annelie Nordin, Lars-Göran Nilsson, Peter De Rijk, Dirk Goossens, Rolf Adolfsson, David M St Clair, Jeremy Hall, Stephen M Lawrie, Andrew M McIntosh, Jurgen Del-Favero, Douglas H R Blackwood, Benjamin S Pickard
Robust statistical, genetic and functional evidence supports a role for DISC1 in the aetiology of major mental illness. Furthermore, many of its protein-binding partners show evidence for involvement in the pathophysiology of a range of neurodevelopmental and psychiatric disorders. Copy number variants (CNVs) are suspected to play an important causal role in these disorders. In this study, CNV analysis of DISC1 and its binding partners PAFAH1B1, NDE1, NDEL1, FEZ1, MAP1A, CIT and PDE4B in Scottish and Northern Swedish population-based samples was carried out using multiplex amplicon quantification...
October 2015: Molecular Neuropsychiatry
Francisco A Moreno, Robert P Erickson, Holly A Garriock, Joel Gelernter, Jim Mintz, Jennifer Oas-Terpstra, Marilyn A Davies, Pedro L Delgado
PURPOSE: The brief and reversible mood response to acute tryptophan (TRP) depletion (ATD) is being studied as a trait marker in subjects considered at risk for major depression (MD). PROCEDURES: ATD was administered to 64 subjects (54 European-Americans, and10 from other races) with personal and family history of MD. They were in remission and had been medication-free for at least three months. Subjects received an active and sham condition in a random assignment, double-blind crossover design...
October 2015: Molecular Neuropsychiatry
Petra Richer, Thomas V Fernandez
Tourette syndrome is a childhood neuropsychiatric disorder, which presents with disruptive motor and vocal tics. The disease also has a high comorbidity with obsessive-compulsive disorder and attention deficit hyperactivity disorder, which may further increase the distress experienced by patients. Current treatments act with varying efficacies in alleviating symptoms, as the underlying biology of the disease is not fully understood to provide precise therapeutic targets. Moreover, the genetic complexity of the disorder presents a substantial challenge to the identification of genetic alterations that contribute to the Tourette's phenotype...
October 2015: Molecular Neuropsychiatry
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