M F Egan

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Building 10, Center Drive, National Institute of Mental Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:6917-22. 2001
  2. ncbi request reprint Relative risk of attention deficits in siblings of patients with schizophrenia
    M F Egan
    NIMH Nueorscience Research Center at St Elizabeth s Hospital, Washington, DC, USA
    Am J Psychiatry 157:1309-16. 2000
  3. ncbi request reprint Relative risk of neurological signs in siblings of patients with schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Intramural Research Program, NIMH, National Institutes of Health, Bethesda, MD, USA
    Am J Psychiatry 158:1827-34. 2001
  4. ncbi request reprint Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression
    R E Straub
    Clinical Brain Disorders Branch, Genes, Cognition, and Psychosis Program, Intramural Research Program, National Institute of Mental Health, NIH, US Department of Health and Human Services, Bethesda, MD 20892 1379, USA
    Mol Psychiatry 12:854-69. 2007
  5. ncbi request reprint Prefrontal neurons and the genetics of schizophrenia
    D R Weinberger
    Clinical Brain Disorders Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 50:825-44. 2001
  6. ncbi request reprint Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics
    S E Bachus
    Clinical Brain Disorders Branch, IRP NIMH NIH, Neuroscience Center at St Elizabeths Hospital, Washington, DC 20032, USA
    J Psychiatr Res 31:233-56. 1997
  7. ncbi request reprint Relative risk for cognitive impairments in siblings of patients with schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 50:98-107. 2001
  8. doi request reprint Serious obstetric complications interact with hypoxia-regulated/vascular-expression genes to influence schizophrenia risk
    K K Nicodemus
    Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 13:873-7. 2008
  9. ncbi request reprint Selective relationship between prefrontal N-acetylaspartate measures and negative symptoms in schizophrenia
    J H Callicott
    Clinical Brain Disorders Branch, Intramural Research Program, NIMH, National Institutes of Health, Bethesda, MD 20892 1389, USA
    Am J Psychiatry 157:1646-51. 2000
  10. ncbi request reprint Evidence for abnormal cortical functional connectivity during working memory in schizophrenia
    A Meyer-Lindenberg
    Unit on Integrative Neuroimaging, Intramural Research Program, NIH, Bethesda, MD 20892 1365, USA
    Am J Psychiatry 158:1809-17. 2001

Detail Information

Publications22

  1. pmc Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Building 10, Center Drive, National Institute of Mental Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:6917-22. 2001
    ..These data suggest that the COMT Val allele, because it increases prefrontal dopamine catabolism, impairs prefrontal cognition and physiology, and by this mechanism slightly increases risk for schizophrenia...
  2. ncbi request reprint Relative risk of attention deficits in siblings of patients with schizophrenia
    M F Egan
    NIMH Nueorscience Research Center at St Elizabeth s Hospital, Washington, DC, USA
    Am J Psychiatry 157:1309-16. 2000
    ..To assess the suitability of impaired attention for use as an intermediate phenotype in genetic studies, the authors estimated the relative risk of impaired attention in a large group of siblings...
  3. ncbi request reprint Relative risk of neurological signs in siblings of patients with schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Intramural Research Program, NIMH, National Institutes of Health, Bethesda, MD, USA
    Am J Psychiatry 158:1827-34. 2001
    ..The authors' goal was to investigate the strength of this possible genetic component...
  4. ncbi request reprint Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression
    R E Straub
    Clinical Brain Disorders Branch, Genes, Cognition, and Psychosis Program, Intramural Research Program, National Institute of Mental Health, NIH, US Department of Health and Human Services, Bethesda, MD 20892 1379, USA
    Mol Psychiatry 12:854-69. 2007
    ..These coincident results implicate GAD1 in the etiology of schizophrenia and suggest that the mechanism involves altered cortical GABA inhibitory activity, perhaps modulated by dopaminergic function...
  5. ncbi request reprint Prefrontal neurons and the genetics of schizophrenia
    D R Weinberger
    Clinical Brain Disorders Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 50:825-44. 2001
    ....
  6. ncbi request reprint Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics
    S E Bachus
    Clinical Brain Disorders Branch, IRP NIMH NIH, Neuroscience Center at St Elizabeths Hospital, Washington, DC 20032, USA
    J Psychiatr Res 31:233-56. 1997
    ..In so far as CCK is co-localized with GABA or glutamate in cortical neurons, both of these neuronal populations need to be studied further in schizophrenia and suicide...
  7. ncbi request reprint Relative risk for cognitive impairments in siblings of patients with schizophrenia
    M F Egan
    Clinical Brain Disorders Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 50:98-107. 2001
    ..Using this dimensional approach to subdividing schizophrenia may reduce the clinical and genetic heterogeneity of schizophrenia and improve the power of genetic studies...
  8. doi request reprint Serious obstetric complications interact with hypoxia-regulated/vascular-expression genes to influence schizophrenia risk
    K K Nicodemus
    Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 13:873-7. 2008
    ....
  9. ncbi request reprint Selective relationship between prefrontal N-acetylaspartate measures and negative symptoms in schizophrenia
    J H Callicott
    Clinical Brain Disorders Branch, Intramural Research Program, NIMH, National Institutes of Health, Bethesda, MD 20892 1389, USA
    Am J Psychiatry 157:1646-51. 2000
    ..The authors hypothesized that an in vivo measure of prefrontal neuronal pathology (N:-acetylaspartate [NAA] levels) in patients with schizophrenia would predict negative symptoms...
  10. ncbi request reprint Evidence for abnormal cortical functional connectivity during working memory in schizophrenia
    A Meyer-Lindenberg
    Unit on Integrative Neuroimaging, Intramural Research Program, NIH, Bethesda, MD 20892 1365, USA
    Am J Psychiatry 158:1809-17. 2001
    ..The authors applied to schizophrenia a recently available functional neuroimaging analytic method that permits characterization of cooperative action on the systems level...
  11. doi request reprint Evidence of biologic epistasis between BDNF and SLC6A4 and implications for depression
    L Pezawas
    Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 13:709-16. 2008
    ....
  12. ncbi request reprint Paired-associate learning and memory interference in schizophrenia
    B Elvevåg
    Clinical Brain Disorders Branch, National Institute of Mental Health National Institutes of Health, Room 4S235 MSC 1379, Building 10, Bethesda, MD 20892, USA
    Neuropsychologia 38:1565-75. 2000
    ..We suggest that the susceptibility to these interference effects in patients with schizophrenia is not a specific problem in cognition, but rather one that is confounded by general memory problems...
  13. ncbi request reprint An association between reduced interhemispheric EEG coherence in the temporal lobe and genetic risk for schizophrenia
    G Winterer
    Clinical Brain Disorder Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1379, USA
    Schizophr Res 49:129-43. 2001
    ..Thus, while power spectrum EEG abnormalities may be state-dependent, reduced coherence as a possible measure of neuronal synchronization is familial and potentially a heritable trait related to genetic risk for schizophrenia...
  14. ncbi request reprint Basal ganglia iron in tardive dyskinesia: an MRI study
    A M Elkashef
    Neuropsychiatry Branch, NIMH, St Elizabeths Hospital, Washington, DC 20032
    Biol Psychiatry 35:16-21. 1994
    ..This suggests that iron deposition in the basal ganglia, at least as assessed by this measure, does not play a role in the pathophysiology of tardive dyskinesia...
  15. ncbi request reprint Memory for temporal order in patients with schizophrenia
    B Elvevåg
    Clinical Brain Disorders Branch, National Institutes of Mental Health National Institute of Health, Bethesda, MD 20892, USA
    Schizophr Res 46:187-93. 2000
    ..e., recall). It is possible that both impairments are due to some third process that underlies and aids in the reconstruction of episodes...
  16. ncbi request reprint Genetic variation in MAOA modulates ventromedial prefrontal circuitry mediating individual differences in human personality
    J W Buckholtz
    Neuroimaging Core Facility, National Institute for Mental Health, NIH, DHHS, Bethesda, MD 20892 1365, USA
    Mol Psychiatry 13:313-24. 2008
    ....
  17. ncbi request reprint Neurobiology of schizophrenia
    M F Egan
    Clinical Research Services, National Institute of Mental Health, Neuroscience Research Center at St Elizabeths, Washington, D C 20032, USA
    Curr Opin Neurobiol 7:701-7. 1997
    ..The use of neurobiological traits as phenotypes, such as cognitive deficits and cortical abnormalities, in genetic linkage studies may facilitate the identification of loci that underlie the most debilitating features of schizophrenia...
  18. ncbi request reprint Neuregulin1-induced cell migration is impaired in schizophrenia: association with neuregulin1 and catechol-o-methyltransferase gene polymorphisms
    Y Sei
    Clinical Brain Disorder Branch, Genes, Cognition, and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1385, USA
    Mol Psychiatry 12:946-57. 2007
    ....
  19. pmc The Premorbid Adjustment Scale as a measure of developmental compromise in patients with schizophrenia and their healthy siblings
    D I Shapiro
    Clinical Brain Disorders Branch, Genes, Cognition, and Psychosis Program, National Institute of Mental Health NIH, 10 Center Drive, Bethesda, MD 20892 1379, USA
    Schizophr Res 112:136-42. 2009
    ..The results suggest that both patients and many of their siblings share poor adjustment in childhood and adolescence, possibly due to shared genetic or environmental risk factors...
  20. ncbi request reprint Effects of smoking during antipsychotic withdrawal in patients with chronic schizophrenia
    J A Apud
    Neuroscience Center at St Elizabeth s, Neuropsychiatry Branch, National Institute of Mental Health, 2700 Martin Luther King, Jr Ave, SE, Washington, DC 20032, USA
    Schizophr Res 46:119-27. 2000
    ..In conclusion, at baseline, smokers had more positive symptoms and were apparently more functionally impaired than non-smokers. This difference was no longer evident after a 30 day medication discontinuation period...
  21. ncbi request reprint Event-related potentials and genetic risk for schizophrenia
    G Winterer
    Clinical Brain Disorders Branch, NIMH/NIH, Building 10, Room 4S229A MSC, Bethesda, MD 20892, USA
    Biol Psychiatry 50:407-17. 2001
    ..Possible reasons for these largely negative findings are discussed...
  22. ncbi request reprint Poor evidence for depolarization block but uncoupling of nigral from striatal dopamine metabolism after chronic haloperidol treatment in the rat
    S J Chrapusta
    Department of Experimental Pharmacology, Polish Academy of Sciences Medical Research Center, Warsaw, Poland
    J Neural Transm 113:573-82. 2006
    ..These results suggest that chronic haloperidol treatment uncouples somatodendritic dopamine turnover and release from those in the axon terminals of nigrostriatal dopamine neurons...