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  1. Article ; Online: Hippocampal Shape and Volume Changes with Antipsychotics in Early-Stage Psychotic Illness

    DanielMamah / MartinAndreasStyner / JeffreyLieberman / LeiWang

    Frontiers in Psychiatry, Vol

    2012  Volume 3

    Abstract: Progression of hippocampal shape and volume abnormalities has been described in psychotic disorders such as schizophrenia. However it is unclear how specific antipsychotic medications influence the development of hippocampal structure. We conducted a ... ...

    Abstract Progression of hippocampal shape and volume abnormalities has been described in psychotic disorders such as schizophrenia. However it is unclear how specific antipsychotic medications influence the development of hippocampal structure. We conducted a longitudinal, randomized, controlled, multisite, double-blind study involving 14 academic medical centers (United States 11, Canada 1, Netherlands 1, and England 1). 134 first-episode psychosis (receiving either haloperidol or olanzapine) patients and 51 healthy controls were treated and followed up for up to 104 weeks using magnetic resonance imaging and large-deformation high-dimensional brain mapping of the hippocampus. Changes in hippocampal volume and shape metrics (i.e., percentage of negative surface vertex slopes, and surface deformation) were evaluated. Mixed-models analysis did not show a significant group-by-time interaction for hippocampal volume. However, the cumulative distribution function of hippocampal surface vertex slopes showed a notable left shift with haloperidol treatment compared to olanzapine treatment and to controls. Olanzapine treatment was associated with a significantly lower percentage of “large magnitude” negative surface vertex slopes compared to haloperidol treatment (p=0.004). Surface deformation maps however did not localize any hippocampal regions that differentially contracted over time with olanzapine treatment, after FDR correction. These results indicate that surface analysis provides supplementary information to volumetry in detecting differential treatment effects of the hippocampus. Our results suggest that olanzapine is associated with less longitudinal hippocampal surface deformation than haloperidol, however the hippocampal regions affected appear to be variable across patients.
    Keywords Haloperidol ; Hippocampus ; Schizophrenia ; psychosis ; morphology ; olanzapine ; Psychiatry ; RC435-571 ; Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R
    Subject code 150 ; 616
    Language English
    Publishing date 2012-11-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: A multicenter study of ketamine effects on functional connectivity

    Leah M. Fleming / Daniel C. Javitt / Cameron S. Carter / Joshua T. Kantrowitz / Ragy R. Girgis / Lawrence S. Kegeles / John D. Ragland / Richard J. Maddock / Tyler A. Lesh / Costin Tanase / James Robinson / William Z. Potter / Marlene Carlson / Melanie M. Wall / Tse-Hwei Choo / Jack Grinband / Jeffrey Lieberman / John H. Krystal / Philip R. Corlett

    NeuroImage: Clinical, Vol 22, Iss , Pp - (2019)

    Large scale network relationships, hubs and symptom mechanisms

    2019  

    Abstract: Ketamine is an uncompetitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist. It induces effects in healthy individuals that mimic symptoms associated with schizophrenia. We sought to root these experiences in altered brain function, ... ...

    Abstract Ketamine is an uncompetitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist. It induces effects in healthy individuals that mimic symptoms associated with schizophrenia. We sought to root these experiences in altered brain function, specifically aberrant resting state functional connectivity (rsfMRI). In the present study, we acquired rsfMRI data under ketamine and placebo in a between-subjects design and analyzed seed-based measures of rsfMRI using large-scale networks, dorsolateral prefrontal cortex (DLPFC) and sub-nuclei of the thalamus. We found ketamine-induced alterations in rsfMRI connectivity similar to those seen in patients with schizophrenia, some changes that may be more comparable to early stages of schizophrenia, and other connectivity signatures seen in patients that ketamine did not recreate. We do not find any circuits from our regions of interest that correlates with positive symptoms of schizophrenia in our sample, although we find that DLPFC connectivity with ACC does correlate with a mood measure. These results provide support for ketamine's use as a model of certain biomarkers of schizophrenia, particularly for early or at-risk patients. Keywords: Ketamine, Functional connectivity, Psychosis, Resting state
    Keywords Computer applications to medicine. Medical informatics ; R858-859.7 ; Neurology. Diseases of the nervous system ; RC346-429
    Subject code 150
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Diretrizes da Federação Mundial das Sociedades de Psiquiatria Biológica para o tratamento biológico da esquizofrenia. Parte 1

    Peter Falkai / Thomas Wobrock / Jeffrey Lieberman / Birte Glenthoj / Wagner F. Gattaz / Hans-Jürgen Möller

    Archives of Clinical Psychiatry, Vol 33, Pp 7-

    tratamento agudo World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of schizophrenia. Part 1: acute treatment

    2006  Volume 64

    Abstract: Estas diretrizes para o tratamento biológico da esquizofrenia foram desenvolvidas pela Força-Tarefa da Federação Mundial das Sociedades de Psiquiatria Biológica (World Federation of Societies of Biological Psychiatry, WFSBP). A meta fixada durante o ... ...

    Abstract Estas diretrizes para o tratamento biológico da esquizofrenia foram desenvolvidas pela Força-Tarefa da Federação Mundial das Sociedades de Psiquiatria Biológica (World Federation of Societies of Biological Psychiatry, WFSBP). A meta fixada durante o desenvolvimento destas diretrizes foi rever sistematicamente todas as evidências disponíveis referentes ao tratamento da esquizofrenia, tanto no âmbito clínico como científico, e chegar a um consenso sobre as principais recomendações para a prática psiquiátrica. Estas diretrizes são destinadas a todos os médicos que atendem e tratam de pacientes portadores de esquizofrenia. Os dados usados para desenvolver estas diretrizes foram extraídos primariamente de vários painéis e diretrizes nacionais de tratamento para esquizofrenia, assim como de metanálises, revisões e estudos clínicos randomizados sobre a eficácia do tratamento farmacológico e de outras intervenções terapêuticas biológicas, identificadas por uma busca nas bases de dados MedLine e Biblioteca Cochrane. A literatura identificada foi avaliada no que diz respeito à solidez das evidências a favor da eficácia de uma dada intervenção e, então, categorizada em quatro níveis de evidências (de A a D). A primeira parte das diretrizes abrange a definição da doença, sua classificação, a epidemiologia e o curso da esquizofrenia, assim como o manejo terapêutico de fase aguda. Estas diretrizes são primariamente relacionadas ao tratamento biológico de adultos esquizofrênicos, incluindo medicação antipsicótica, outras opções de tratamento farmacológico, terapia eletroconvulsiva, estratégias terapêuticas recentes e complementares. These guidelines for the biological treatment of schizophrenia were developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). The goal during the development of these guidelines was to review systematically all available evidence pertaining to the treatment of schizophrenia, and to reach a consensus on a series of practice recommendations that are clinically and scientifically meaningful based on the available evidence. These guidelines are intended for use by all physicians seeing and treating people with schizophrenia. The data used for developing these guidelines have been extracted primarily from various national treatment guidelines and panels for schizophrenia, as well as from meta-analyses, reviews and randomised clinical trials on the efficacy of pharmacological and other biological treatment interventions identified by a search of the MEDLINE database and Cochrane Library. The identified literature was evaluated with respect to the strength of evidence for its efficacy and then categorised into four levels of evidence (A/D). This first part of the guidelines covers disease definition, classification, epidemiology and course of schizophrenia, as well as the management of the acute phase treatment. These guidelines are primarily concerned with the biological treatment (including antipsychotic medication, other pharmacological treatment options, electroconvulsive therapy, adjunctive and novel therapeutic strategies) of adults suffering from schizophrenia.
    Keywords Esquizofrenia ; Tratamento da fase aguda ; Medicina baseada em evidências ; Diretrizes práticas ; Tratamento biológico ; Antipsicóticos ; Schizophrenia ; Acute phase treatment ; Evidence-based medicine ; Practice guidelines ; Biological treatment ; Antipsychotics ; Psychiatry ; RC435-571
    Language English
    Publishing date 2006-01-01T00:00:00Z
    Publisher Universidade de São Paulo
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Diretrizes da Federação Mundial das Sociedades de Psiquiatria Biológica para o tratamento biológico da esquizofrenia. Parte 2

    Peter Falkai / Thomas Wobrock / Jeffrey Lieberman / Birte Glenthoj / Wagner F. Gattaz / Hans-Jürgen Möller

    Archives of Clinical Psychiatry, Vol 33, Pp 65-

    tratamento de longo prazo World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of schizophrenia. Part 2: long-term treatment

    2006  Volume 100

    Abstract: Estas diretrizes para o tratamento biológico da esquizofrenia foram desenvolvidas pela Força-Tarefa da Federação Mundial das Sociedades de Psiquiatria Biológica (World Federation of Societies of Biological Psychiatry, WFSBP). As metas fixadas durante o ... ...

    Abstract Estas diretrizes para o tratamento biológico da esquizofrenia foram desenvolvidas pela Força-Tarefa da Federação Mundial das Sociedades de Psiquiatria Biológica (World Federation of Societies of Biological Psychiatry, WFSBP). As metas fixadas durante o desenvolvimento destas diretrizes foi a revisão sistemática de todas as evidências disponíveis referentes ao tratamento da esquizofrenia, tanto no âmbito clínico como no científico, e o estabelecimento de um consenso sobre as principais recomendações para a prática psiquiátrica. Estas diretrizes são destinadas a todos os médicos que atendem e tratam de pacientes portadores de esquizofrenia. Os dados usados para desenvolver estas diretrizes foram extraídos primariamente de vários painéis e diretrizes nacionais para o tratamento da esquizofrenia, assim como de metanálises, revisões e estudos clínicos randomizados sobre a eficácia do tratamento farmacológico e de outras intervenções terapêuticas biológicas, identificadas por uma busca nas bases de dados MedLine e na Biblioteca Cochrane. A literatura identificada foi avaliada quanto à solidez das evidências a favor da eficácia de determinada intervenção, sendo, então, categorizada em quatro níveis de evidência (de A a D). A segunda parte das diretrizes abrange o tratamento de longo prazo, bem como o controle dos efeitos colaterais relevantes. Essas diretrizes são primariamente relacionadas ao tratamento biológico de adultos esquizofrênicos, incluindo medicação antipsicótica, outras opções de tratamento farmacológico, eletroconvulsoterapia, estratégias terapêuticas recentes e complementares. These guidelines for the biological treatment of schizophrenia were developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). The goal during the development of these guidelines was to review systematically all available evidence pertaining to the treatment of schizophrenia, and to reach a consensus on a series of practice recommendations that are clinically and scientifically meaningful based on the available evidence. These guidelines are intended for use by all physicians seeing and treating people with schizophrenia. The data used for developing these guidelines have been extracted primarily from various national treatment guidelines and panels for schizophrenia, as well as from meta-analyses, reviews and randomised clinical trials on the efficacy of pharmacological and other biological treatment interventions identified by a search of the MEDLINE database and Cochrane Library. The identified literature was evaluated with respect to the strength of evidence for its efficacy and then categorised into four levels of evidence (A/D). This second part of the guidelines covers the long-term treatment as well as the management of relevant side effects. These guidelines are primarily concerned with the biological treatment (including antipsychotic medication, other pharmacological treatment options, electroconvulsive therapy, adjunctive and novel therapeutic strategies) of adults suffering from schizophrenia.
    Keywords Esquizofrenia ; Tratamento da fase aguda ; Medicina baseada em evidências ; Diretrizes práticas ; Tratamento biológico ; Antipsicóticos ; Schizophrenia ; Long-term treatment ; Evidence-based medicine ; Practice guidelines ; Biological treatment ; Antipsychotics ; Psychiatry ; RC435-571
    Language English
    Publishing date 2006-01-01T00:00:00Z
    Publisher Universidade de São Paulo
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Using brain cell-type-specific protein interactomes to interpret neurodevelopmental genetic signals in schizophrenia

    Yu-Han H. Hsu / Greta Pintacuda / Ruize Liu / Eugeniu Nacu / April Kim / Kalliopi Tsafou / Natalie Petrossian / William Crotty / Jung Min Suh / Jackson Riseman / Jacqueline M. Martin / Julia C. Biagini / Daya Mena / Joshua K.T. Ching / Edyta Malolepsza / Taibo Li / Tarjinder Singh / Tian Ge / Shawn B. Egri /
    Benjamin Tanenbaum / Caroline R. Stanclift / Annie M. Apffel / Steven A. Carr / Monica Schenone / Jake Jaffe / Nadine Fornelos / Hailiang Huang / Kevin C. Eggan / Kasper Lage / Stephan Ripke / Benjamin M. Neale / Aiden Corvin / James T.R. Walters / Kai-How Farh / Peter A. Holmans / Phil Lee / Brendan Bulik-Sullivan / David A. Collier / Tune H. Pers / Ingrid Agartz / Esben Agerbo / Margot Albus / Madeline Alexander / Farooq Amin / Silviu A. Bacanu / Martin Begemann / Richard A. Belliveau, Jr. / Judit Bene / Sarah E. Bergen / Elizabeth Bevilacqua / Tim B. Bigdeli / Donald W. Black / Richard Bruggeman / Nancy G. Buccola / Randy L. Buckner / William Byerley / Wiepke Cahn / Guiqing Cai / Dominique Campion / Rita M. Cantor / Vaughan J. Carr / Noa Carrera / Stanley V. Catts / Kimberley D. Chambert / Raymond C.K. Chan / Ronald Y.L. Chan / Eric Y.H. Chen / Wei Cheng / Eric FC. Cheung / Siow Ann Chong / C. Robert Cloninger / David Cohen / Nadine Cohen / Paul Cormican / Nick Craddock / James J. Crowley / David Curtis / Michael Davidson / Kenneth L. Davis / Franziska Degenhardt / Jurgen Del Favero / Ditte Demontis / Dimitris Dikeos / Timothy Dinan / Srdjan Djurovic / Gary Donohoe / Elodie Drapeau / Jubao Duan / Frank Dudbridge / Naser Durmishi / Peter Eichhammer / Johan Eriksson / Valentina Escott-Price / Laurent Essioux / Ayman H. Fanous / Martilias S. Farrell / Josef Frank / Lude Franke / Robert Freedman / Nelson B. Freimer / Marion Friedl / Joseph I. Friedman / Menachem Fromer / Giulio Genovese / Lyudmila Georgieva / Ina Giegling / Paola Giusti-Rodríguez / Stephanie Godard / Jacqueline I. Goldstein / Vera Golimbet / Srihari Gopal / Jacob Gratten / Lieuwe de Haan / Christian Hammer / Marian L. Hamshere / Mark Hansen / Thomas Hansen / Vahram Haroutunian / Annette M. Hartmann / Frans A. Henskens / Stefan Herms / Joel N. Hirschhorn / Per Hoffmann / Andrea Hofman / Mads V. Hollegaard / David M. Hougaard / Masashi Ikeda / Inge Joa / Antonio Julià / René S. Kahn / Luba Kalaydjieva / Sena Karachanak-Yankova / Juha Karjalainen / David Kavanagh / Matthew C. Keller / James L. Kennedy / Andrey Khrunin / Yunjung Kim / Janis Klovins / James A. Knowles / Bettina Konte / Vaidutis Kucinskas / Zita Ausrele Kucinskiene / Hana Kuzelova-Ptackova / Anna K. Kähler / Claudine Laurent / Jimmy Lee / S. Hong Lee / Sophie E. Legge / Bernard Lerer / Miaoxin Li / Tao Li / Kung-Yee Liang / Jeffrey Lieberman / Svetlana Limborska / Carmel M. Loughland / Jan Lubinski / Jouko Lönnqvist / Milan Macek / Patrik K.E. Magnusson / Brion S. Maher / Wolfgang Maier / Jacques Mallet / Sara Marsal / Manuel Mattheisen / Morten Mattingsdal / Robert W. McCarley / Colm McDonald / Andrew M. McIntosh / Sandra Meier / Carin J. Meijer / Bela Melegh / Ingrid Melle / Raquelle I. Mesholam-Gately / Andres Metspalu / Patricia T. Michie / Lili Milani / Vihra Milanova / Younes Mokrab / Derek W. Morris / Ole Mors / Kieran C. Murphy / Robin M. Murray / Inez Myin-Germeys / Bertram Müller-Myhsok / Mari Nelis / Igor Nenadic / Deborah A. Nertney / Gerald Nestadt / Kristin K. Nicodemus / Liene Nikitina-Zake / Laura Nisenbaum / Annelie Nordin / Eadbhard O'Callaghan / Colm O'Dushlaine / F. Anthony O'Neill / Sang-Yun Oh / Ann Olincy / Line Olsen / Jim Van Os / Christos Pantelis / George N. Papadimitriou / Sergi Papiol / Elena Parkhomenko / Michele T. Pato / Tiina Paunio / Milica Pejovic-Milovancevic / Diana O. Perkins / Olli Pietiläinen / Jonathan Pimm / Andrew J. Pocklington / John Powell / Alkes Price / Ann E. Pulver / Shaun M. Purcell / Digby Quested / Henrik B. Rasmussen / Abraham Reichenberg / Mark A. Reimers / Alexander L. Richards / Joshua L. Roffman / Panos Roussos / Douglas M. Ruderfer / Veikko Salomaa / Alan R. Sanders / Ulrich Schall / Christian R. Schubert / Thomas G. Schulze / Sibylle G. Schwab / Edward M. Scolnick / Rodney J. Scott / Larry J. Seidman / Jianxin Shi / Engilbert Sigurdsson / Teimuraz Silagadze / Jeremy M. Silverman / Kang Sim / Petr Slominsky / Jordan W. Smoller / Hon-Cheong So / Chris C.A. Spencer / Eli A. Stahl / Hreinn Stefansson / Stacy Steinberg / Elisabeth Stogmann / Richard E. Straub / Eric Strengman / Jana Strohmaier / T Scott Stroup / Mythily Subramaniam / Jaana Suvisaari / Dragan M. Svrakic / Jin P. Szatkiewicz / Erik Söderman / Srinivas Thirumalai / Draga Toncheva / Sarah Tosato / Juha Veijola / John Waddington / Dermot Walsh / Dai Wang / Qiang Wang / Bradley T. Webb / Mark Weiser / Dieter B. Wildenauer / Nigel M. Williams / Stephanie Williams / Stephanie H. Witt / Aaron R. Wolen / Emily H.M. Wong / Brandon K. Wormley / Hualin Simon Xi / Clement C. Zai / Xuebin Zheng / Fritz Zimprich / Naomi R. Wray / Kari Stefansson / Peter M. Visscher / Rolf Adolfsson / Ole A. Andreassen / Douglas H.R. Blackwood / Elvira Bramon / Joseph D. Buxbaum / Anders D. Børglum / Sven Cichon / Ariel Darvasi / Enrico Domenici / Hannelore Ehrenreich / Tõnu Esko / Pablo V. Gejman / Michael Gill / Hugh Gurling / Christina M. Hultman / Nakao Iwata / Assen V. Jablensky / Erik G. Jönsson / Kenneth S. Kendler / George Kirov / Jo Knight / Todd Lencz / Douglas F. Levinson / Qingqin S. Li / Jianjun Liu / Anil K. Malhotra / Steven A. McCarroll / Andrew McQuillin / Jennifer L. Moran / Preben B. Mortensen / Bryan J. Mowry / Markus M. Nöthen / Roel A. Ophoff / Michael J. Owen / Aarno Palotie / Carlos N. Pato / Tracey L. Petryshen / Danielle Posthuma / Marcella Rietschel / Brien P. Riley / Dan Rujescu / Pak C. Sham / Pamela Sklar / David St Clair / Daniel R. Weinberger / Jens R. Wendland / Thomas Werge / Mark J. Daly / Patrick F. Sullivan / Michael C. O'Donovan / Shengying Qin / Akira Sawa / Rene Kahn / Kyung Sue Hong / Wenzhao Shi / Ming Tsuang / Masanari Itokawa / Gang Feng / Stephen J. Glatt / Xiancang Ma / Jinsong Tang / Yunfeng Ruan / Feng Zhu / Yasue Horiuchi / Byung Dae Lee / Eun-Jeong Joo / Woojae Myung / Kyooseob Ha / Hong-Hee Won / Ji Hyung Baek / Young Chul Chung / Sung-Wan Kim / Agung Kusumawardhani / Wei J. Chen / Hai-Gwo Hwu / Akitoyo Hishimoto / Ikuo Otsuka / Ichiro Sora / Tomoko Toyota / Takeo Yoshikawa / Hiroshi Kunugi / Kotaro Hattori / Sayuri Ishiwata / Shusuke Numata / Tetsuro Ohmori / Makoto Arai / Yuji Ozeki / Kumiko Fujii / Se Joo Kim / Heon-Jeong Lee / Yong Min Ahn / Se Hyun Kim / Kazufumi Akiyama / Kazutaka Shimoda / Makoto Kinoshita

    iScience, Vol 26, Iss 5, Pp 106701- (2023)

    2023  

    Abstract: Summary: Genetics have nominated many schizophrenia risk genes and identified convergent signals between schizophrenia and neurodevelopmental disorders. However, functional interpretation of the nominated genes in the relevant brain cell types is often ... ...

    Abstract Summary: Genetics have nominated many schizophrenia risk genes and identified convergent signals between schizophrenia and neurodevelopmental disorders. However, functional interpretation of the nominated genes in the relevant brain cell types is often lacking. We executed interaction proteomics for six schizophrenia risk genes that have also been implicated in neurodevelopment in human induced cortical neurons. The resulting protein network is enriched for common variant risk of schizophrenia in Europeans and East Asians, is down-regulated in layer 5/6 cortical neurons of individuals affected by schizophrenia, and can complement fine-mapping and eQTL data to prioritize additional genes in GWAS loci. A sub-network centered on HCN1 is enriched for common variant risk and contains proteins (HCN4 and AKAP11) enriched for rare protein-truncating mutations in individuals with schizophrenia and bipolar disorder. Our findings showcase brain cell-type-specific interactomes as an organizing framework to facilitate interpretation of genetic and transcriptomic data in schizophrenia and its related disorders.
    Keywords Molecular interaction ; Developmental neuroscience ; Cellular neuroscience ; Proteomics ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2023-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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