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  1. AU="Brohawn, David G"
  2. AU="Cho, Chun-Chieh"
  3. AU="van Raalte, Daniël H"
  4. AU="Zargarian, Loussiné"
  5. AU=Hascalovici Jacob
  6. AU="Spagnolo, Jennifer B"
  7. AU="Anderloni, Giulia"
  8. AU="Ahmad, Shoaib"
  9. AU="Du, Roujia"
  10. AU="Colmenero-Repiso, Ana"
  11. AU="Alvarez-Carbonell, David"
  12. AU="Phelippeau, Michael"
  13. AU="Lunghi, Laura"
  14. AU=Giersiepen Klaus
  15. AU="Drobyshev, Sergey"
  16. AU="Timme, Kathleen H"
  17. AU=Sfriso Paolo
  18. AU="Kim, John S"
  19. AU=Farkash Evan A AU=Farkash Evan A
  20. AU="Xia, Xueqian"

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  1. Artikel: RNA Sequencing Reveals Small and Variable Contributions of Infectious Agents to Transcriptomes of Postmortem Nervous Tissues From Amyotrophic Lateral Sclerosis, Alzheimer's Disease and Parkinson's Disease Subjects, and Increased Expression of Genes From Disease-Activated Microglia.

    Bennett, James P / Keeney, Paula M / Brohawn, David G

    Frontiers in neuroscience

    2019  Band 13, Seite(n) 235

    Abstract: Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show ... ...

    Abstract Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), show activated microglia, suggesting a potential causal role for inflammation in pathogenesis of NDD. We performed paired-end (PE) RNA sequencing (RNA seq) of total RNA's extracted from frozen sections of cervical spinal cords from ALS and CTL subjects, frontal cortical gray matter ribbons of AD and CTL subjects, and ventral midbrains of PD and CTL subjects. Trimmed PE reads were aligned against the hg38 human transcriptome using Tophat2/Bowtie2 (ALS) or HISAT2 (AD and PD) and quantitated with Cufflinks. PE reads were also aligned using Bowtie2 against genomes from representative species of
    Sprache Englisch
    Erscheinungsdatum 2019-03-28
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2019.00235
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: RNAseq Analyses Identify Tumor Necrosis Factor-Mediated Inflammation as a Major Abnormality in ALS Spinal Cord.

    Brohawn, David G / O'Brien, Laura C / Bennett, James P

    PloS one

    2016  Band 11, Heft 8, Seite(n) e0160520

    Abstract: ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular ... ...

    Abstract ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular insights into pathogenesis and progression are sorely needed. In that context, we used high-depth, next generation RNA sequencing (RNAseq, Illumina) to define gene network abnormalities in RNA samples depleted of rRNA and isolated from cervical spinal cord sections of 7 ALS and 8 CTL samples. We aligned >50 million 2X150 bp paired-end sequences/sample to the hg19 human genome and applied three different algorithms (Cuffdiff2, DEseq2, EdgeR) for identification of differentially expressed genes (DEG's). Ingenuity Pathways Analysis (IPA) and Weighted Gene Co-expression Network Analysis (WGCNA) identified inflammatory processes as significantly elevated in our ALS samples, with tumor necrosis factor (TNF) found to be a major pathway regulator (IPA) and TNFα-induced protein 2 (TNFAIP2) as a major network "hub" gene (WGCNA). Using the oPOSSUM algorithm, we analyzed transcription factors (TF) controlling expression of the nine DEG/hub genes in the ALS samples and identified TF's involved in inflammation (NFkB, REL, NFkB1) and macrophage function (NR1H2::RXRA heterodimer). Transient expression in human iPSC-derived motor neurons of TNFAIP2 (also a DEG identified by all three algorithms) reduced cell viability and induced caspase 3/7 activation. Using high-density RNAseq, multiple algorithms for DEG identification, and an unsupervised gene co-expression network approach, we identified significant elevation of inflammatory processes in ALS spinal cord with TNF as a major regulatory molecule. Overexpression of the DEG TNFAIP2 in human motor neurons, the population most vulnerable to die in ALS, increased cell death and caspase 3/7 activation. We propose that therapies targeted to reduce inflammatory TNFα signaling may be helpful in ALS patients.
    Mesh-Begriff(e) Amyotrophic Lateral Sclerosis/complications ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/pathology ; Autopsy ; Case-Control Studies ; Gene Regulatory Networks ; Genome-Wide Association Study ; High-Throughput Nucleotide Sequencing ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Sequence Analysis, RNA ; Signal Transduction/genetics ; Spinal Cord/immunology ; Spinal Cord/metabolism ; Spinal Cord/pathology ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/physiology
    Chemische Substanzen TNF protein, human ; Tumor Necrosis Factor-alpha
    Sprache Englisch
    Erscheinungsdatum 2016
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0160520
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Pharmacological properties of microneurotrophin drugs developed for treatment of amyotrophic lateral sclerosis.

    Bennett, James P / O'Brien, Laura C / Brohawn, David G

    Biochemical pharmacology

    2016  Band 117, Seite(n) 68–77

    Abstract: Microneurotrophins (MNT's) are small molecule derivatives of dehydroepiandrosterone (DHEA) and do not have significant interactions with sex steroid receptors. MNT's retain high-affinity binding to protein tyrosine kinase (Trk) receptors and can mimic ... ...

    Abstract Microneurotrophins (MNT's) are small molecule derivatives of dehydroepiandrosterone (DHEA) and do not have significant interactions with sex steroid receptors. MNT's retain high-affinity binding to protein tyrosine kinase (Trk) receptors and can mimic many pleiotropic actions of neurotrophin (NT) proteins on neurons. MNT's offer therapeutic potential for diseases such as amyotrophic lateral sclerosis (ALS) where motor neurons (MN) degenerate. MNT's cross artificial membranes mimicking the blood-brain barrier, are not major substrates for ABC (ATP-binding cassette) transporters and are metabolized rapidly by mouse but more slowly by human hepatocytes. A lead MNT (BNN27) and its mono-oxidation metabolites enter mouse brain rapidly. RNA-sequencing measured gene expression profiles of human H9eSC-(embryonic stem cell)-derived or CTL (control) subject iPSC-(induced pluripotential stem cell)-derived MN's exposed to NT proteins or MNT molecules. Expression ratios (relative to DMSO (dimethylsulfoxide) vehicle) were calculated, and the resulting top 500 gene lists were analyzed for Gene Ontology (GO) grouping using DAVID (Database for Annotation, Visualization and Integrated Discovery). The MNT's BNN20, BNN23, and BNN27 showed overlap of GO terms with NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor) in the H9eSC-derived MN's. In the iPSC-derived MN's two (BNN20, BNN27) showed overlap of GO terms with NGF or BDNF. Each NT protein had GO terms that did not overlap with any MNT in the MN cell lines.
    Mesh-Begriff(e) ATP Binding Cassette Transporter, Sub-Family B/antagonists & inhibitors ; ATP Binding Cassette Transporter, Sub-Family B/genetics ; ATP Binding Cassette Transporter, Sub-Family B/metabolism ; Absorption, Physiological/drug effects ; Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Animals ; Biotransformation ; Blood-Brain Barrier ; Caco-2 Cells ; Cell Line ; Cells, Cultured ; Dehydroepiandrosterone/analogs & derivatives ; Dehydroepiandrosterone/metabolism ; Dehydroepiandrosterone/pharmacokinetics ; Dehydroepiandrosterone/pharmacology ; Dogs ; Drugs, Investigational/metabolism ; Drugs, Investigational/pharmacokinetics ; Drugs, Investigational/pharmacology ; Gene Expression Regulation/drug effects ; Hepatocytes/cytology ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/drug effects ; Madin Darby Canine Kidney Cells ; Membrane Transport Modulators/pharmacology ; Mice ; Motor Neurons/cytology ; Motor Neurons/drug effects ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neuroprotective Agents/metabolism ; Neuroprotective Agents/pharmacokinetics ; Neuroprotective Agents/pharmacology ; Recombinant Proteins/chemistry ; Recombinant Proteins/metabolism ; Tissue Distribution
    Chemische Substanzen ABCB1 protein, human ; ATP Binding Cassette Transporter, Sub-Family B ; BNN20 compound ; BNN23 compound ; BNN27 compound ; Drugs, Investigational ; Membrane Transport Modulators ; Nerve Tissue Proteins ; Neuroprotective Agents ; Recombinant Proteins ; Dehydroepiandrosterone (459AG36T1B)
    Sprache Englisch
    Erscheinungsdatum 2016-10-01
    Erscheinungsland England
    Dokumenttyp Comparative Study ; Journal Article
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2016.08.001
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: RNA-seq analyses reveal that cervical spinal cords and anterior motor neurons from amyotrophic lateral sclerosis subjects show reduced expression of mitochondrial DNA-encoded respiratory genes, and rhTFAM may correct this respiratory deficiency.

    Ladd, Amy C / Brohawn, David G / Thomas, Ravindar R / Keeney, Paula M / Berr, Stuart S / Khan, Shaharyar M / Portell, Francisco R / Shakenov, Meiram Zh / Antkowiak, Patrick F / Kundu, Bijoy / Tustison, Nicholas / Bennett, James P

    Brain research

    2017  Band 1667, Seite(n) 74–83

    Abstract: Amyotrophic lateral sclerosis (ALS) is a generally fatal neurodegenerative disease of adults that produces weakness and atrophy due to dysfunction and death of upper and lower motor neurons. We used RNA-sequencing (RNA-seq) to analyze expression of all ... ...

    Abstract Amyotrophic lateral sclerosis (ALS) is a generally fatal neurodegenerative disease of adults that produces weakness and atrophy due to dysfunction and death of upper and lower motor neurons. We used RNA-sequencing (RNA-seq) to analyze expression of all mitochondrial DNA (mtDNA)-encoded respiratory genes in ALS and CTL human cervical spinal cords (hCSC) and isolated motor neurons. We analyzed with RNA-seq mtDNA gene expression in human neural stem cells (hNSC) exposed to recombinant human mitochondrial transcription factor A (rhTFAM), visualized in 3-dimensions clustered gene networks activated by rhTFAM, quantitated their interactions with other genes and determined their gene ontology (GO) families. RNA-seq and quantitative PCR (qPCR) analyses showed reduced mitochondrial gene expression in ALS hCSC and ALS motor neurons isolated by laser capture microdissection (LCM), and revealed that hNSC and CTL human cervical spinal cords were similar. Rats treated with i.v. rhTFAM showed a dose-response increase in brain respiration and an increase in spinal cord mitochondrial gene expression. Treatment of hNSC with rhTFAM increased expression of mtDNA-encoded respiratory genes and produced one major and several minor clusters of gene interactions. Gene ontology (GO) analysis of rhTFAM-stimulated gene clusters revealed enrichment in GO families involved in RNA and mRNA metabolism, suggesting mitochondrial-nuclear signaling. In postmortem ALS hCSC and LCM-isolated motor neurons we found reduced expression of mtDNA respiratory genes. In hNSC's rhTFAM increased mtDNA gene expression and stimulated mRNA metabolism by unclear mechanisms. rhTFAM may be useful in improving bioenergetic function in ALS.
    Mesh-Begriff(e) Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Brain/diagnostic imaging ; Brain/metabolism ; Cells, Cultured ; Cervical Cord/metabolism ; DNA, Mitochondrial ; DNA-Binding Proteins/administration & dosage ; DNA-Binding Proteins/metabolism ; Gene Expression ; Glucose/metabolism ; Humans ; Laser Capture Microdissection ; Male ; Mitochondrial Proteins/administration & dosage ; Mitochondrial Proteins/metabolism ; Motor Neurons/metabolism ; Neural Stem Cells/metabolism ; Rats, Sprague-Dawley ; Recombinant Proteins/administration & dosage ; Recombinant Proteins/metabolism ; Sequence Analysis, RNA ; Transcription Factors/administration & dosage ; Transcription Factors/metabolism
    Chemische Substanzen DNA, Mitochondrial ; DNA-Binding Proteins ; Mitochondrial Proteins ; Recombinant Proteins ; Transcription Factors ; mitochondrial transcription factor A ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2017-05-13
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2017.05.010
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Genetic variation throughout the folate metabolic pathway influences negative symptom severity in schizophrenia.

    Roffman, Joshua L / Brohawn, David G / Nitenson, Adam Z / Macklin, Eric A / Smoller, Jordan W / Goff, Donald C

    Schizophrenia bulletin

    2011  Band 39, Heft 2, Seite(n) 330–338

    Abstract: Low serum folate levels previously have been associated with negative symptom risk in schizophrenia, as has the hypofunctional 677C>T variant of the MTHFR gene. This study examined whether other missense polymorphisms in folate-regulating enzymes, in ... ...

    Abstract Low serum folate levels previously have been associated with negative symptom risk in schizophrenia, as has the hypofunctional 677C>T variant of the MTHFR gene. This study examined whether other missense polymorphisms in folate-regulating enzymes, in concert with MTHFR, influence negative symptoms in schizophrenia, and whether total risk allele load interacts with serum folate status to further stratify negative symptom risk. Medicated outpatients with schizophrenia (n = 219), all of European origin and some included in a previous report, were rated with the Positive and Negative Syndrome Scale. A subset of 82 patients also underwent nonfasting serum folate testing. Patients were genotyped for the MTHFR 677C>T (rs1801133), MTHFR 1298A>C (rs1801131), MTR 2756A>G (rs1805087), MTRR 203A>G (rs1801394), FOLH1 484T>C (rs202676), RFC 80A>G (rs1051266), and COMT 675G>A (rs4680) polymorphisms. All genotypes were entered into a linear regression model to determine significant predictors of negative symptoms, and risk scores were calculated based on total risk allele dose. Four variants, MTHFR 677T, MTR 2756A, FOLH1 484C, and COMT 675A, emerged as significant independent predictors of negative symptom severity, accounting for significantly greater variance in negative symptoms than MTHFR 677C>T alone. Total allele dose across the 4 variants predicted negative symptom severity only among patients with low folate levels. These findings indicate that multiple genetic variants within the folate metabolic pathway contribute to negative symptoms of schizophrenia. A relationship between folate level and negative symptom severity among patients with greater genetic vulnerability is biologically plausible and suggests the utility of folate supplementation in these patients.
    Mesh-Begriff(e) 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase/genetics ; Adult ; Catechol O-Methyltransferase/genetics ; Cohort Studies ; Female ; Ferredoxin-NADP Reductase/genetics ; Folic Acid/blood ; Folic Acid/metabolism ; Gene Frequency ; Genetic Predisposition to Disease ; Glutamate Carboxypeptidase II/genetics ; Humans ; Linear Models ; Male ; Metabolic Networks and Pathways/genetics ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Mutation, Missense ; Polymorphism, Single Nucleotide ; Reduced Folate Carrier Protein/genetics ; Schizophrenia/genetics ; Schizophrenia/metabolism ; Schizophrenic Psychology ; Severity of Illness Index
    Chemische Substanzen Reduced Folate Carrier Protein ; SLC19A1 protein, human ; Folic Acid (935E97BOY8) ; methionine synthase reductase (EC 1.18.1.-) ; Ferredoxin-NADP Reductase (EC 1.18.1.2) ; MTHFR protein, human (EC 1.5.1.20) ; Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20) ; 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase (EC 2.1.1.13) ; Catechol O-Methyltransferase (EC 2.1.1.6) ; Glutamate Carboxypeptidase II (EC 3.4.17.21)
    Sprache Englisch
    Erscheinungsdatum 2011-10-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 439173-1
    ISSN 1745-1701 ; 0586-7614
    ISSN (online) 1745-1701
    ISSN 0586-7614
    DOI 10.1093/schbul/sbr150
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: MTHFR 677C>T effects on anterior cingulate structure and function during response monitoring in schizophrenia: a preliminary study

    Roffman, Joshua L / Brohawn, David G / Friedman, Jesse S / Dyckman, Kara A / Thakkar, Katharine N / Agam, Yigal / Vangel, Mark G / Goff, Donald C / Manoach, Dara S

    Brain imaging and behavior. 2011 Mar., v. 5, no. 1

    2011  

    Abstract: Patients with schizophrenia exhibit deficient response monitoring as indexed by blunted activation of the dorsal anterior cingulate cortex (dACC) and functionally related regions during error commission. This pattern may reflect heritable alterations of ... ...

    Abstract Patients with schizophrenia exhibit deficient response monitoring as indexed by blunted activation of the dorsal anterior cingulate cortex (dACC) and functionally related regions during error commission. This pattern may reflect heritable alterations of dACC function. We examined whether the hypofunctional 677C>T variant in MTHFR, a candidate schizophrenia risk gene, contributed to our previous findings of blunted error-related dACC activation and reduced microstructural integrity of dACC white matter. Eighteen medicated outpatients with schizophrenia underwent diffusion tensor imaging and performed an antisaccade paradigm during functional magnetic resonance imaging (fMRI). T allele carriers exhibited significantly less error-related activation than C/C patients in bilateral dACC and substantia nigra, regions that are thought to mediate dopamine-dependent error-based reinforcement learning. T carrier patients also showed significantly lower fractional anisotropy in bilateral dACC. These findings suggest that the MTHFR 677T allele blunts response monitoring in schizophrenia, presumably via effects on dopamine signaling and dACC white matter microstructural integrity.
    Schlagwörter genetics
    Sprache Englisch
    Erscheinungsverlauf 2011-03
    Umfang p. 65-75.
    Verlag Springer-Verlag
    Erscheinungsort New York
    Dokumenttyp Artikel
    ZDB-ID 2377165-3
    ISSN 1931-7565 ; 1931-7557
    ISSN (online) 1931-7565
    ISSN 1931-7557
    DOI 10.1007/s11682-010-9111-2
    Datenquelle NAL Katalog (AGRICOLA)

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  7. Artikel ; Online: A hypomethylating variant of MTHFR, 677C>T, blunts the neural response to errors in patients with schizophrenia and healthy individuals.

    Roffman, Joshua L / Nitenson, Adam Z / Agam, Yigal / Isom, Marlisa / Friedman, Jesse S / Dyckman, Kara A / Brohawn, David G / Smoller, Jordan W / Goff, Donald C / Manoach, Dara S

    PloS one

    2011  Band 6, Heft 9, Seite(n) e25253

    Abstract: Background: Responding to errors is a critical first step in learning from mistakes, a process that is abnormal in schizophrenia. To gain insight into the neural and molecular mechanisms of error processing, we used functional MRI to examine effects of ... ...

    Abstract Background: Responding to errors is a critical first step in learning from mistakes, a process that is abnormal in schizophrenia. To gain insight into the neural and molecular mechanisms of error processing, we used functional MRI to examine effects of a genetic variant in methylenetetrahydrofolate reductase (MTHFR 677C>T, rs1801133) that increases risk for schizophrenia and that has been specifically associated with increased perseverative errors among patients. MTHFR is a key regulator of the intracellular one-carbon milieu, including DNA methylation, and each copy of the 677T allele reduces MTHFR activity by 35%.
    Methodology/principal findings: Using an antisaccade paradigm, we found that the 677T allele induces a dose-dependent blunting of dorsal anterior cingulate cortex (dACC) activation in response to errors, a pattern that was identical in healthy individuals and patients with schizophrenia. Further, the normal relationship between dACC activation and error rate was disrupted among carriers of the 677T allele.
    Conclusions/significance: These findings implicate an epigenetic mechanism in the neural response to errors, and provide insight into normal cognitive variation through a schizophrenia risk gene.
    Mesh-Begriff(e) Adult ; Alleles ; DNA Methylation/genetics ; Female ; Genetic Predisposition to Disease ; Humans ; Magnetic Resonance Imaging ; Male ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Methylenetetrahydrofolate Reductase (NADPH2)/metabolism ; Schizophrenia/genetics
    Chemische Substanzen Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20)
    Sprache Englisch
    Erscheinungsdatum 2011-09-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0025253
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: MTHFR 677C>T effects on anterior cingulate structure and function during response monitoring in schizophrenia: a preliminary study.

    Roffman, Joshua L / Brohawn, David G / Friedman, Jesse S / Dyckman, Kara A / Thakkar, Katharine N / Agam, Yigal / Vangel, Mark G / Goff, Donald C / Manoach, Dara S

    Brain imaging and behavior

    2010  Band 5, Heft 1, Seite(n) 65–75

    Abstract: Patients with schizophrenia exhibit deficient response monitoring as indexed by blunted activation of the dorsal anterior cingulate cortex (dACC) and functionally related regions during error commission. This pattern may reflect heritable alterations of ... ...

    Abstract Patients with schizophrenia exhibit deficient response monitoring as indexed by blunted activation of the dorsal anterior cingulate cortex (dACC) and functionally related regions during error commission. This pattern may reflect heritable alterations of dACC function. We examined whether the hypofunctional 677C>T variant in MTHFR, a candidate schizophrenia risk gene, contributed to our previous findings of blunted error-related dACC activation and reduced microstructural integrity of dACC white matter. Eighteen medicated outpatients with schizophrenia underwent diffusion tensor imaging and performed an antisaccade paradigm during functional magnetic resonance imaging (fMRI). T allele carriers exhibited significantly less error-related activation than C/C patients in bilateral dACC and substantia nigra, regions that are thought to mediate dopamine-dependent error-based reinforcement learning. T carrier patients also showed significantly lower fractional anisotropy in bilateral dACC. These findings suggest that the MTHFR 677T allele blunts response monitoring in schizophrenia, presumably via effects on dopamine signaling and dACC white matter microstructural integrity.
    Mesh-Begriff(e) Adult ; Alleles ; Anisotropy ; Corpus Striatum/pathology ; Diagnostic and Statistical Manual of Mental Disorders ; Diffusion Magnetic Resonance Imaging ; Feedback, Psychological/physiology ; Female ; Genotype ; Gyrus Cinguli/pathology ; Gyrus Cinguli/physiology ; Humans ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging ; Male ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Psychomotor Performance/physiology ; Saccades/physiology ; Schizophrenia/genetics ; Schizophrenia/pathology ; Schizophrenic Psychology ; Substantia Nigra/pathology
    Chemische Substanzen Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20)
    Sprache Englisch
    Erscheinungsdatum 2010-12-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2377165-3
    ISSN 1931-7565 ; 1931-7557
    ISSN (online) 1931-7565
    ISSN 1931-7557
    DOI 10.1007/s11682-010-9111-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Identification of common variants associated with human hippocampal and intracranial volumes.

    Stein, Jason L / Medland, Sarah E / Vasquez, Alejandro Arias / Hibar, Derrek P / Senstad, Rudy E / Winkler, Anderson M / Toro, Roberto / Appel, Katja / Bartecek, Richard / Bergmann, Ørjan / Bernard, Manon / Brown, Andrew A / Cannon, Dara M / Chakravarty, M Mallar / Christoforou, Andrea / Domin, Martin / Grimm, Oliver / Hollinshead, Marisa / Holmes, Avram J /
    Homuth, Georg / Hottenga, Jouke-Jan / Langan, Camilla / Lopez, Lorna M / Hansell, Narelle K / Hwang, Kristy S / Kim, Sungeun / Laje, Gonzalo / Lee, Phil H / Liu, Xinmin / Loth, Eva / Lourdusamy, Anbarasu / Mattingsdal, Morten / Mohnke, Sebastian / Maniega, Susana Muñoz / Nho, Kwangsik / Nugent, Allison C / O'Brien, Carol / Papmeyer, Martina / Pütz, Benno / Ramasamy, Adaikalavan / Rasmussen, Jerod / Rijpkema, Mark / Risacher, Shannon L / Roddey, J Cooper / Rose, Emma J / Ryten, Mina / Shen, Li / Sprooten, Emma / Strengman, Eric / Teumer, Alexander / Trabzuni, Daniah / Turner, Jessica / van Eijk, Kristel / van Erp, Theo G M / van Tol, Marie-Jose / Wittfeld, Katharina / Wolf, Christiane / Woudstra, Saskia / Aleman, Andre / Alhusaini, Saud / Almasy, Laura / Binder, Elisabeth B / Brohawn, David G / Cantor, Rita M / Carless, Melanie A / Corvin, Aiden / Czisch, Michael / Curran, Joanne E / Davies, Gail / de Almeida, Marcio A A / Delanty, Norman / Depondt, Chantal / Duggirala, Ravi / Dyer, Thomas D / Erk, Susanne / Fagerness, Jesen / Fox, Peter T / Freimer, Nelson B / Gill, Michael / Göring, Harald H H / Hagler, Donald J / Hoehn, David / Holsboer, Florian / Hoogman, Martine / Hosten, Norbert / Jahanshad, Neda / Johnson, Matthew P / Kasperaviciute, Dalia / Kent, Jack W / Kochunov, Peter / Lancaster, Jack L / Lawrie, Stephen M / Liewald, David C / Mandl, René / Matarin, Mar / Mattheisen, Manuel / Meisenzahl, Eva / Melle, Ingrid / Moses, Eric K / Mühleisen, Thomas W / Nauck, Matthias / Nöthen, Markus M / Olvera, Rene L / Pandolfo, Massimo / Pike, G Bruce / Puls, Ralf / Reinvang, Ivar / Rentería, Miguel E / Rietschel, Marcella / Roffman, Joshua L / Royle, Natalie A / Rujescu, Dan / Savitz, Jonathan / Schnack, Hugo G / Schnell, Knut / Seiferth, Nina / Smith, Colin / Steen, Vidar M / Valdés Hernández, Maria C / Van den Heuvel, Martijn / van der Wee, Nic J / Van Haren, Neeltje E M / Veltman, Joris A / Völzke, Henry / Walker, Robert / Westlye, Lars T / Whelan, Christopher D / Agartz, Ingrid / Boomsma, Dorret I / Cavalleri, Gianpiero L / Dale, Anders M / Djurovic, Srdjan / Drevets, Wayne C / Hagoort, Peter / Hall, Jeremy / Heinz, Andreas / Jack, Clifford R / Foroud, Tatiana M / Le Hellard, Stephanie / Macciardi, Fabio / Montgomery, Grant W / Poline, Jean Baptiste / Porteous, David J / Sisodiya, Sanjay M / Starr, John M / Sussmann, Jessika / Toga, Arthur W / Veltman, Dick J / Walter, Henrik / Weiner, Michael W / Bis, Joshua C / Ikram, M Arfan / Smith, Albert V / Gudnason, Vilmundur / Tzourio, Christophe / Vernooij, Meike W / Launer, Lenore J / DeCarli, Charles / Seshadri, Sudha / Andreassen, Ole A / Apostolova, Liana G / Bastin, Mark E / Blangero, John / Brunner, Han G / Buckner, Randy L / Cichon, Sven / Coppola, Giovanni / de Zubicaray, Greig I / Deary, Ian J / Donohoe, Gary / de Geus, Eco J C / Espeseth, Thomas / Fernández, Guillén / Glahn, David C / Grabe, Hans J / Hardy, John / Hulshoff Pol, Hilleke E / Jenkinson, Mark / Kahn, René S / McDonald, Colm / McIntosh, Andrew M / McMahon, Francis J / McMahon, Katie L / Meyer-Lindenberg, Andreas / Morris, Derek W / Müller-Myhsok, Bertram / Nichols, Thomas E / Ophoff, Roel A / Paus, Tomas / Pausova, Zdenka / Penninx, Brenda W / Potkin, Steven G / Sämann, Philipp G / Saykin, Andrew J / Schumann, Gunter / Smoller, Jordan W / Wardlaw, Joanna M / Weale, Michael E / Martin, Nicholas G / Franke, Barbara / Wright, Margaret J / Thompson, Paul M

    Nature genetics

    2012  Band 44, Heft 5, Seite(n) 552–561

    Abstract: Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in ... ...

    Abstract Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 × 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 × 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 × 10(-7)).
    Mesh-Begriff(e) Brain/physiopathology ; Chromosomes, Human, Pair 12/genetics ; Genetic Loci ; Genetic Markers ; Genome-Wide Association Study ; Hippocampus/physiopathology ; Humans ; Meta-Analysis as Topic ; Neuroimaging ; Polymorphism, Single Nucleotide/genetics
    Chemische Substanzen Genetic Markers
    Sprache Englisch
    Erscheinungsdatum 2012-04-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng.2250
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: The ENIGMA Consortium: large-scale collaborative analyses of neuroimaging and genetic data.

    Thompson, Paul M / Stein, Jason L / Medland, Sarah E / Hibar, Derrek P / Vasquez, Alejandro Arias / Renteria, Miguel E / Toro, Roberto / Jahanshad, Neda / Schumann, Gunter / Franke, Barbara / Wright, Margaret J / Martin, Nicholas G / Agartz, Ingrid / Alda, Martin / Alhusaini, Saud / Almasy, Laura / Almeida, Jorge / Alpert, Kathryn / Andreasen, Nancy C /
    Andreassen, Ole A / Apostolova, Liana G / Appel, Katja / Armstrong, Nicola J / Aribisala, Benjamin / Bastin, Mark E / Bauer, Michael / Bearden, Carrie E / Bergmann, Orjan / Binder, Elisabeth B / Blangero, John / Bockholt, Henry J / Bøen, Erlend / Bois, Catherine / Boomsma, Dorret I / Booth, Tom / Bowman, Ian J / Bralten, Janita / Brouwer, Rachel M / Brunner, Han G / Brohawn, David G / Buckner, Randy L / Buitelaar, Jan / Bulayeva, Kazima / Bustillo, Juan R / Calhoun, Vince D / Cannon, Dara M / Cantor, Rita M / Carless, Melanie A / Caseras, Xavier / Cavalleri, Gianpiero L / Chakravarty, M Mallar / Chang, Kiki D / Ching, Christopher R K / Christoforou, Andrea / Cichon, Sven / Clark, Vincent P / Conrod, Patricia / Coppola, Giovanni / Crespo-Facorro, Benedicto / Curran, Joanne E / Czisch, Michael / Deary, Ian J / de Geus, Eco J C / den Braber, Anouk / Delvecchio, Giuseppe / Depondt, Chantal / de Haan, Lieuwe / de Zubicaray, Greig I / Dima, Danai / Dimitrova, Rali / Djurovic, Srdjan / Dong, Hongwei / Donohoe, Gary / Duggirala, Ravindranath / Dyer, Thomas D / Ehrlich, Stefan / Ekman, Carl Johan / Elvsåshagen, Torbjørn / Emsell, Louise / Erk, Susanne / Espeseth, Thomas / Fagerness, Jesen / Fears, Scott / Fedko, Iryna / Fernández, Guillén / Fisher, Simon E / Foroud, Tatiana / Fox, Peter T / Francks, Clyde / Frangou, Sophia / Frey, Eva Maria / Frodl, Thomas / Frouin, Vincent / Garavan, Hugh / Giddaluru, Sudheer / Glahn, David C / Godlewska, Beata / Goldstein, Rita Z / Gollub, Randy L / Grabe, Hans J / Grimm, Oliver / Gruber, Oliver / Guadalupe, Tulio / Gur, Raquel E / Gur, Ruben C / Göring, Harald H H / Hagenaars, Saskia / Hajek, Tomas / Hall, Geoffrey B / Hall, Jeremy / Hardy, John / Hartman, Catharina A / Hass, Johanna / Hatton, Sean N / Haukvik, Unn K / Hegenscheid, Katrin / Heinz, Andreas / Hickie, Ian B / Ho, Beng-Choon / Hoehn, David / Hoekstra, Pieter J / Hollinshead, Marisa / Holmes, Avram J / Homuth, Georg / Hoogman, Martine / Hong, L Elliot / Hosten, Norbert / Hottenga, Jouke-Jan / Hulshoff Pol, Hilleke E / Hwang, Kristy S / Jack, Clifford R / Jenkinson, Mark / Johnston, Caroline / Jönsson, Erik G / Kahn, René S / Kasperaviciute, Dalia / Kelly, Sinead / Kim, Sungeun / Kochunov, Peter / Koenders, Laura / Krämer, Bernd / Kwok, John B J / Lagopoulos, Jim / Laje, Gonzalo / Landen, Mikael / Landman, Bennett A / Lauriello, John / Lawrie, Stephen M / Lee, Phil H / Le Hellard, Stephanie / Lemaître, Herve / Leonardo, Cassandra D / Li, Chiang-Shan / Liberg, Benny / Liewald, David C / Liu, Xinmin / Lopez, Lorna M / Loth, Eva / Lourdusamy, Anbarasu / Luciano, Michelle / Macciardi, Fabio / Machielsen, Marise W J / Macqueen, Glenda M / Malt, Ulrik F / Mandl, René / Manoach, Dara S / Martinot, Jean-Luc / Matarin, Mar / Mather, Karen A / Mattheisen, Manuel / Mattingsdal, Morten / Meyer-Lindenberg, Andreas / McDonald, Colm / McIntosh, Andrew M / McMahon, Francis J / McMahon, Katie L / Meisenzahl, Eva / Melle, Ingrid / Milaneschi, Yuri / Mohnke, Sebastian / Montgomery, Grant W / Morris, Derek W / Moses, Eric K / Mueller, Bryon A / Muñoz Maniega, Susana / Mühleisen, Thomas W / Müller-Myhsok, Bertram / Mwangi, Benson / Nauck, Matthias / Nho, Kwangsik / Nichols, Thomas E / Nilsson, Lars-Göran / Nugent, Allison C / Nyberg, Lars / Olvera, Rene L / Oosterlaan, Jaap / Ophoff, Roel A / Pandolfo, Massimo / Papalampropoulou-Tsiridou, Melina / Papmeyer, Martina / Paus, Tomas / Pausova, Zdenka / Pearlson, Godfrey D / Penninx, Brenda W / Peterson, Charles P / Pfennig, Andrea / Phillips, Mary / Pike, G Bruce / Poline, Jean-Baptiste / Potkin, Steven G / Pütz, Benno / Ramasamy, Adaikalavan / Rasmussen, Jerod / Rietschel, Marcella / Rijpkema, Mark / Risacher, Shannon L / Roffman, Joshua L / Roiz-Santiañez, Roberto / Romanczuk-Seiferth, Nina / Rose, Emma J / Royle, Natalie A / Rujescu, Dan / Ryten, Mina / Sachdev, Perminder S / Salami, Alireza / Satterthwaite, Theodore D / Savitz, Jonathan / Saykin, Andrew J / Scanlon, Cathy / Schmaal, Lianne / Schnack, Hugo G / Schork, Andrew J / Schulz, S Charles / Schür, Remmelt / Seidman, Larry / Shen, Li / Shoemaker, Jody M / Simmons, Andrew / Sisodiya, Sanjay M / Smith, Colin / Smoller, Jordan W / Soares, Jair C / Sponheim, Scott R / Sprooten, Emma / Starr, John M / Steen, Vidar M / Strakowski, Stephen / Strike, Lachlan / Sussmann, Jessika / Sämann, Philipp G / Teumer, Alexander / Toga, Arthur W / Tordesillas-Gutierrez, Diana / Trabzuni, Daniah / Trost, Sarah / Turner, Jessica / Van den Heuvel, Martijn / van der Wee, Nic J / van Eijk, Kristel / van Erp, Theo G M / van Haren, Neeltje E M / van 't Ent, Dennis / van Tol, Marie-Jose / Valdés Hernández, Maria C / Veltman, Dick J / Versace, Amelia / Völzke, Henry / Walker, Robert / Walter, Henrik / Wang, Lei / Wardlaw, Joanna M / Weale, Michael E / Weiner, Michael W / Wen, Wei / Westlye, Lars T / Whalley, Heather C / Whelan, Christopher D / White, Tonya / Winkler, Anderson M / Wittfeld, Katharina / Woldehawariat, Girma / Wolf, Christiane / Zilles, David / Zwiers, Marcel P / Thalamuthu, Anbupalam / Schofield, Peter R / Freimer, Nelson B / Lawrence, Natalia S / Drevets, Wayne

    Brain imaging and behavior

    2014  Band 8, Heft 2, Seite(n) 153–182

    Abstract: The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups ... ...

    Abstract The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,171 individuals were provided by the CHARGE consortium for replication of findings, in a total of 24,997 subjects. By meta-analyzing results from many sites, ENIGMA has detected factors that affect the brain that no individual site could detect on its own, and that require larger numbers of subjects than any individual neuroimaging study has currently collected. ENIGMA's first project was a genome-wide association study identifying common variants in the genome associated with hippocampal volume or intracranial volume. Continuing work is exploring genetic associations with subcortical volumes (ENIGMA2) and white matter microstructure (ENIGMA-DTI). Working groups also focus on understanding how schizophrenia, bipolar illness, major depression and attention deficit/hyperactivity disorder (ADHD) affect the brain. We review the current progress of the ENIGMA Consortium, along with challenges and unexpected discoveries made on the way.
    Mesh-Begriff(e) Brain Mapping/methods ; Cooperative Behavior ; Genome-Wide Association Study/methods ; Humans ; Meta-Analysis as Topic ; Neuroimaging/methods
    Sprache Englisch
    Erscheinungsdatum 2014-01-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2377165-3
    ISSN 1931-7565 ; 1931-7557
    ISSN (online) 1931-7565
    ISSN 1931-7557
    DOI 10.1007/s11682-013-9269-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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