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Molecular Psychiatry

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https://www.readbyqxmd.com/read/29467497/altered-taok2-activity-causes-autism-related-neurodevelopmental-and-cognitive-abnormalities-through-rhoa-signaling
#1
Melanie Richter, Nadeem Murtaza, Robin Scharrenberg, Sean H White, Ole Johanns, Susan Walker, Ryan K C Yuen, Birgit Schwanke, Bianca Bedürftig, Melad Henis, Sarah Scharf, Vanessa Kraus, Ronja Dörk, Jakob Hellmann, Zsuzsa Lindenmaier, Jacob Ellegood, Henrike Hartung, Vickie Kwan, Jan Sedlacik, Jens Fiehler, Michaela Schweizer, Jason P Lerch, Ileana L Hanganu-Opatz, Fabio Morellini, Stephen W Scherer, Karun K Singh, Froylan Calderon de Anda
Atypical brain connectivity is a major contributor to the pathophysiology of neurodevelopmental disorders (NDDs) including autism spectrum disorders (ASDs). TAOK2 is one of several genes in the 16p11.2 microdeletion region, but whether it contributes to NDDs is unknown. We performed behavioral analysis on Taok2 heterozygous (Het) and knockout (KO) mice and found gene dosage-dependent impairments in cognition, anxiety, and social interaction. Taok2 Het and KO mice also have dosage-dependent abnormalities in brain size and neural connectivity in multiple regions, deficits in cortical layering, dendrite and synapse formation, and reduced excitatory neurotransmission...
February 21, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29463886/a-set-of-regulatory-genes-co-expressed-in-embryonic-human-brain-is-implicated-in-disrupted-speech-development
#2
Else Eising, Amaia Carrion-Castillo, Arianna Vino, Edythe A Strand, Kathy J Jakielski, Thomas S Scerri, Michael S Hildebrand, Richard Webster, Alan Ma, Bernard Mazoyer, Clyde Francks, Melanie Bahlo, Ingrid E Scheffer, Angela T Morgan, Lawrence D Shriberg, Simon E Fisher
Genetic investigations of people with impaired development of spoken language provide windows into key aspects of human biology. Over 15 years after FOXP2 was identified, most speech and language impairments remain unexplained at the molecular level. We sequenced whole genomes of nineteen unrelated individuals diagnosed with childhood apraxia of speech, a rare disorder enriched for causative mutations of large effect. Where DNA was available from unaffected parents, we discovered de novo mutations, implicating genes, including CHD3, SETD1A and WDR5...
February 20, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29459796/genetic-inhibition-of-neurotransmission-reveals-role-of-glutamatergic-input-to-dopamine-neurons-in-high-effort-behavior
#3
M A Hutchison, X Gu, M F Adrover, M R Lee, T S Hnasko, V A Alvarez, W Lu
This corrects the article DOI: 10.1038/mp.2017.7.
February 20, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29453413/depression-and-obesity-evidence-of-shared-biological-mechanisms
#4
REVIEW
Yuri Milaneschi, W Kyle Simmons, Elisabeth F C van Rossum, Brenda Wjh Penninx
Depression and obesity are common conditions with major public health implications that tend to co-occur within individuals. The relationship between these conditions is bidirectional: the presence of one increases the risk for developing the other. It has thus become crucial to gain a better understanding of the mechanisms responsible for the intertwined downward physiological spirals associated with both conditions. The present review focuses specifically on shared biological pathways that may mechanistically explain the depression-obesity link, including genetics, alterations in systems involved in homeostatic adjustments (HPA axis, immuno-inflammatory activation, neuroendocrine regulators of energy metabolism including leptin and insulin, and microbiome) and brain circuitries integrating homeostatic and mood regulatory responses...
February 16, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29449635/purkinje-cells-derived-from-tsc-patients-display-hypoexcitability-and-synaptic-deficits-associated-with-reduced-fmrp-levels-and-reversed-by-rapamycin
#5
Maria Sundberg, Ivan Tochitsky, David E Buchholz, Kellen Winden, Ville Kujala, Kush Kapur, Deniz Cataltepe, Daria Turner, Min-Joon Han, Clifford J Woolf, Mary E Hatten, Mustafa Sahin
Accumulating evidence suggests that cerebellar dysfunction early in life is associated with autism spectrum disorder (ASD), but the molecular mechanisms underlying the cerebellar deficits at the cellular level are unclear. Tuberous sclerosis complex (TSC) is a neurocutaneous disorder that often presents with ASD. Here, we developed a cerebellar Purkinje cell (PC) model of TSC with patient-derived human induced pluripotent stem cells (hiPSCs) to characterize the molecular mechanisms underlying cerebellar abnormalities in ASD and TSC...
February 15, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29426955/uncoupling-the-widespread-occurrence-of-anti-nmdar1-autoantibodies-from-neuropsychiatric-disease-in-a-novel-autoimmune-model
#6
Hong Pan, Bárbara Oliveira, Gesine Saher, Ekrem Dere, Daniel Tapken, Marina Mitjans, Jan Seidel, Janina Wesolowski, Debia Wakhloo, Christina Klein-Schmidt, Anja Ronnenberg, Kerstin Schwabe, Ralf Trippe, Kerstin Mätz-Rensing, Stefan Berghoff, Yazeed Al-Krinawe, Henrik Martens, Martin Begemann, Winfried Stöcker, Franz-Josef Kaup, Reinhard Mischke, Susann Boretius, Klaus-Armin Nave, Joachim K Krauss, Michael Hollmann, Fred Lühder, Hannelore Ehrenreich
Autoantibodies of the IgG class against N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1-AB) were considered pathognomonic for anti-NMDAR encephalitis. This view has been challenged by the age-dependent seroprevalence (up to >20%) of functional NMDAR1-AB of all immunoglobulin classes found in >5000 individuals, healthy or affected by different diseases. These findings question a merely encephalitogenic role of NMDAR1-AB. Here, we show that NMDAR1-AB belong to the normal autoimmune repertoire of dogs, cats, rats, mice, baboons, and rhesus macaques, and are functional in the NMDAR1 internalization assay based on human IPSC-derived cortical neurons...
February 9, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29426954/3d-7li-magnetic-resonance-imaging-of-brain-lithium-distribution-in-bipolar-disorder
#7
Fiona Elizabeth Smith, Peter Edward Thelwall, Joe Necus, Carly Jay Flowers, Andrew Matthew Blamire, David Andrew Cousins
Lithium is a major treatment for bipolar disorder and the likelihood of a favourable response may be determined by its distribution in the brain. Lithium can be directly detected by magnetic resonance (MR), but previous 7Li MR spectroscopy studies have demonstrated that this is challenging compared to conventional 1H MR imaging due to the MR properties of the lithium nucleus and its low concentration in brain tissue, as dictated by therapeutic dose. We have tested and implemented a highly efficient balanced steady-state free precession 7Li-MRI method to address these challenges and enable MRI of brain lithium in a short duration scan...
February 9, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29422521/the-pulvinar-nucleus-and-antidepressant-treatment-dynamic-modeling-of-antidepressant-response-and-remission-with-ultra-high-field-functional-mri
#8
Kraus Christoph, Klöbl Manfred, Tik Martin, Auer Bastian, Vanicek Thomas, Geissberger Nicole, Daniela M Pfabigan, Hahn Andreas, Woletz Michael, Paul Katharina, Komorowski Arkadiusz, Kasper Siegfried, Windischberger Christian, Lamm Claus, Lanzenberger Rupert
Functional magnetic resonance imaging (fMRI) successfully disentangled neuronal pathophysiology of major depression (MD), but only a few fMRI studies have investigated correlates and predictors of remission. Moreover, most studies have used clinical outcome parameters from two time points, which do not optimally depict differential response times. Therefore, we aimed to detect neuronal correlates of response and remission in an antidepressant treatment study with 7 T fMRI, potentially harnessing advances in detection power and spatial specificity...
February 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29422520/lithium-treatment-and-mechanisms-of-aging
#9
Anthony S Zannas
No abstract text is available yet for this article.
February 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29422519/exercise-induced-hippocampal-neurogenesis-5-ht3-receptor-antagonism-by-antipsychotics-as-a-potential-limiting-factor-in-schizophrenia
#10
LETTER
David D Kim, Alasdair M Barr, William G Honer, Ric M Procyshyn
No abstract text is available yet for this article.
February 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29326435/a-combined-analysis-of-genetically-correlated-traits-identifies-187-loci-and-a-role-for-neurogenesis-and-myelination-in-intelligence
#11
W D Hill, R E Marioni, O Maghzian, S J Ritchie, S P Hagenaars, A M McIntosh, C R Gale, G Davies, I J Deary
Intelligence, or general cognitive function, is phenotypically and genetically correlated with many traits, including a wide range of physical, and mental health variables. Education is strongly genetically correlated with intelligence (r g  = 0.70). We used these findings as foundations for our use of a novel approach-multi-trait analysis of genome-wide association studies (MTAG; Turley et al. 2017)-to combine two large genome-wide association studies (GWASs) of education and intelligence, increasing statistical power and resulting in the largest GWAS of intelligence yet reported...
January 11, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29321673/genomic-analysis-of-family-data-reveals-additional-genetic-effects-on-intelligence-and-personality
#12
W David Hill, Ruben C Arslan, Charley Xia, Michelle Luciano, Carmen Amador, Pau Navarro, Caroline Hayward, Reka Nagy, David J Porteous, Andrew M McIntosh, Ian J Deary, Chris S Haley, Lars Penke
Pedigree-based analyses of intelligence have reported that genetic differences account for 50-80% of the phenotypic variation. For personality traits these effects are smaller, with 34-48% of the variance being explained by genetic differences. However, molecular genetic studies using unrelated individuals typically report a heritability estimate of around 30% for intelligence and between 0 and 15% for personality variables. Pedigree-based estimates and molecular genetic estimates may differ because current genotyping platforms are poor at tagging causal variants, variants with low minor allele frequency, copy number variants, and structural variants...
January 10, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29317742/psychiatric-genetics-and-the-structure-of-psychopathology
#13
REVIEW
Jordan W Smoller, Ole A Andreassen, Howard J Edenberg, Stephen V Faraone, Stephen J Glatt, Kenneth S Kendler
For over a century, psychiatric disorders have been defined by expert opinion and clinical observation. The modern DSM has relied on a consensus of experts to define categorical syndromes based on clusters of symptoms and signs, and, to some extent, external validators, such as longitudinal course and response to treatment. In the absence of an established etiology, psychiatry has struggled to validate these descriptive syndromes, and to define the boundaries between disorders and between normal and pathologic variation...
January 9, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29311665/hippocampal-dysfunction-in-the-pathophysiology-of-schizophrenia-a-selective-review-and-hypothesis-for-early-detection-and-intervention
#14
J A Lieberman, R R Girgis, G Brucato, H Moore, F Provenzano, L Kegeles, D Javitt, J Kantrowitz, M M Wall, C M Corcoran, S A Schobel, S A Small
Scientists have long sought to characterize the pathophysiologic basis of schizophrenia and develop biomarkers that could identify the illness. Extensive postmortem and in vivo neuroimaging research has described the early involvement of the hippocampus in the pathophysiology of schizophrenia. In this context, we have developed a hypothesis that describes the evolution of schizophrenia-from the premorbid through the prodromal stages to syndromal psychosis-and posits dysregulation of glutamate neurotransmission beginning in the CA1 region of the hippocampus as inducing attenuated psychotic symptoms and initiating the transition to syndromal psychosis...
January 9, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29311664/calhm2-governs-astrocytic-atp-releasing-in-the-development-of-depression-like-behaviors
#15
M Jun, Q Xiaolong, Y Chaojuan, P Ruiyuan, W Shukun, W Junbing, H Li, C Hong, C Jinbo, W Rong, L Yajin, M Lanqun, W Fengchao, W Zhiying, A Jianxiong, W Yun, Z Xia, Z Chen, Y Zengqiang
This corrects the article DOI: 10.1038/mp.2017.229.
January 9, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29311653/meta-analysis-of-epigenome-wide-association-studies-of-cognitive-abilities
#16
Riccardo E Marioni, Allan F McRae, Jan Bressler, Elena Colicino, Eilis Hannon, Shuo Li, Diddier Prada, Jennifer A Smith, Letizia Trevisi, Pei-Chien Tsai, Dina Vojinovic, Jeannette Simino, Daniel Levy, Chunyu Liu, Michael Mendelson, Claudia L Satizabal, Qiong Yang, Min A Jhun, Sharon L R Kardia, Wei Zhao, Stefania Bandinelli, Luigi Ferrucci, Dena G Hernandez, Andrew B Singleton, Sarah E Harris, John M Starr, Douglas P Kiel, Robert R McLean, Allan C Just, Joel Schwartz, Avron Spiro, Pantel Vokonas, Najaf Amin, M Arfan Ikram, Andre G Uitterlinden, Joyce B J van Meurs, Tim D Spector, Claire Steves, Andrea A Baccarelli, Jordana T Bell, Cornelia M van Duijn, Myriam Fornage, Yi-Hsiang Hsu, Jonathan Mill, Thomas H Mosley, Sudha Seshadri, Ian J Deary
Cognitive functions are important correlates of health outcomes across the life-course. Individual differences in cognitive functions are partly heritable. Epigenetic modifications, such as DNA methylation, are susceptible to both genetic and environmental factors and may provide insights into individual differences in cognitive functions. Epigenome-wide meta-analyses for blood-based DNA methylation levels at ~420,000 CpG sites were performed for seven measures of cognitive functioning using data from 11 cohorts...
January 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29311652/adult-generated-neurons-born-during-chronic-social-stress-are-uniquely-adapted-to-respond-to-subsequent-chronic-social-stress
#17
Zurine De Miguel, Ursula Haditsch, Theo D Palmer, Arantza Azpiroz, Robert M Sapolsky
Chronic stress is a recognized risk factor for psychiatric and psychological disorders and a potent modulator of adult neurogenesis. Numerous studies have shown that during stress, neurogenesis decreases; however, during the recovery from the stress, neurogenesis increases. Despite the increased number of neurons born after stress, it is unknown if the function and morphology of those neurons are altered. Here we asked whether neurons in adult mice, born during the final 5 days of chronic social stress and matured during recovery from chronic social stress, are similar to neurons born with no stress conditions from a quantitative, functional and morphological perspective, and whether those neurons are uniquely adapted to respond to a subsequent stressful challenge...
January 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29311651/identification-of-a-novel-gene-regulating-amygdala-mediated-fear-extinction
#18
Ozge Gunduz-Cinar, Emma Brockway, Lauren Lederle, Troy Wilcox, Lindsay R Halladay, Ying Ding, Hyunjung Oh, Erica F Busch, Katie Kaugars, Shaun Flynn, Aaron Limoges, Olena Bukalo, Kathryn P MacPherson, Sophie Masneuf, Courtney Pinard, Etienne Sibille, Elissa J Chesler, Andrew Holmes
Recent years have seen advances in our understanding of the neural circuits associated with trauma-related disorders, and the development of relevant assays for these behaviors in rodents. Although inherited factors are known to influence individual differences in risk for these disorders, it has been difficult to identify specific genes that moderate circuit functions to affect trauma-related behaviors. Here, we exploited robust inbred mouse strain differences in Pavlovian fear extinction to uncover quantitative trait loci (QTL) associated with this trait...
January 8, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29302076/candidate-cspg4-mutations-and-induced-pluripotent-stem-cell-modeling-implicate-oligodendrocyte-progenitor-cell-dysfunction-in-familial-schizophrenia
#19
Femke M de Vrij, Christian G Bouwkamp, Nilhan Gunhanlar, Guy Shpak, Bas Lendemeijer, Maarouf Baghdadi, Shreekara Gopalakrishna, Mehrnaz Ghazvini, Tracy M Li, Marialuisa Quadri, Simone Olgiati, Guido J Breedveld, Michiel Coesmans, Edwin Mientjes, Ton de Wit, Frans W Verheijen, H Berna Beverloo, Dan Cohen, Rob M Kok, P Roberto Bakker, Aviva Nijburg, Annet T Spijker, P M Judith Haffmans, Erik Hoencamp, Veerle Bergink, Jacob A Vorstman, Timothy Wu, Loes M Olde Loohuis, Najaf Amin, Carolyn D Langen, Albert Hofman, Witte J Hoogendijk, Cornelia M van Duijn, M Arfan Ikram, Meike W Vernooij, Henning Tiemeier, André G Uitterlinden, Ype Elgersma, Ben Distel, Joost Gribnau, Tonya White, Vincenzo Bonifati, Steven A Kushner
Schizophrenia is highly heritable, yet its underlying pathophysiology remains largely unknown. Among the most well-replicated findings in neurobiological studies of schizophrenia are deficits in myelination and white matter integrity; however, direct etiological genetic and cellular evidence has thus far been lacking. Here, we implement a family-based approach for genetic discovery in schizophrenia combined with functional analysis using induced pluripotent stem cells (iPSCs). We observed familial segregation of two rare missense mutations in Chondroitin Sulfate Proteoglycan 4 (CSPG4) (c...
January 4, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29302075/foxo1-a2m-and-tgf-%C3%AE-1-three-novel-genes-predicting-depression-in-gene-x-environment-interactions-are-identified-using-cross-species-and-cross-tissues-transcriptomic-and-mirnomic-analyses
#20
Annamaria Cattaneo, Nadia Cattane, Chiara Malpighi, Darina Czamara, Anna Suarez, Nicole Mariani, Eero Kajantie, Alessia Luoni, Johan G Eriksson, Jari Lahti, Valeria Mondelli, Paola Dazzan, Katri Räikkönen, Elisabeth B Binder, Marco A Riva, Carmine M Pariante
To date, gene-environment (GxE) interaction studies in depression have been limited to hypothesis-based candidate genes, since genome-wide (GWAS)-based GxE interaction studies would require enormous datasets with genetics, environmental, and clinical variables. We used a novel, cross-species and cross-tissues "omics" approach to identify genes predicting depression in response to stress in GxE interactions. We integrated the transcriptome and miRNome profiles from the hippocampus of adult rats exposed to prenatal stress (PNS) with transcriptome data obtained from blood mRNA of adult humans exposed to early life trauma, using a stringent statistical analyses pathway...
January 4, 2018: Molecular Psychiatry
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