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  • 1
    Online Resource
    Online Resource
    Brain, Behavior and Epigenetics. (2011)
    Berlin, Heidelberg :Springer Berlin / Heidelberg,
    Details
    Keywords: Behavior genetics -- Periodicals. ; Electronic books.
    Description / Table of Contents: Epigenetics, once believed stable after development, has been found to occur in fully differentiated, post-mitotic central nervous system cells in response to environmental signals. This book explores the role of epigenetic risk factors in complex diseases.
    Type of Medium: Online Resource
    Pages: 1 online resource (333 pages)
    Edition: 1st ed.
    ISBN: 9783642174261
    Series Statement: Epigenetics and Human Health Series
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=763423
    DDC: 612.646
    Language: English
    Note: Intro -- CONTENTS -- 1 Posttranslational Histone Modifications and the Neurobiology of Psychosis -- 2 Epigenetic Regulation of GABAergic Targets in Psychiatry -- 3 Possible Roles of DNA Methylation in Bipolar Disorder -- 4 The Epigenetics of Depression and Suicide -- 5 Epidemiology Research and Epigenetics: Translational Epidemiology of Schizophrenia -- 6 Environmental Studies as a Tool for Detecting Epigenetic Mechanisms in Schizophrenia -- 7 Imprinting, Inactivation and the Behavioural Genetics of the X Chromosome -- 8 The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain -- 9 Genomic Imprinting Effects on Brain and Behavior: Future Directions -- 10 Epigenetic Influence of the Social Environment -- 11 Toward an Understanding of the Dynamic Interdependence of Genes and Environment in the Regulation of Phenotype -- 12 Histone Deacetylase Inhibitors: A Novel Therapeutic Approach for Cognitive Disorders -- 13 Epigenetic Mechanisms of Memory Consolidation -- 14 Epigenetic Mechanisms in Memory Formation -- Glossary -- Index.
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  • 2
    Electronic Resource
    Electronic Resource
    Psychosis and genes with trinucleotide repeat polymorphism (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 244-246 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Abnormal expansion of genes with trinucleotide repeat (TNR) polymorphism has been found in a number of neuropsychiatric disorders. These disorders and the major psychoses, schizophrenia and bipolar affective disorder, appear to share an interesting phenomenon: genetic anticipation. Because TNR expansion correlates with anticipation, these unstable DNA sites are considered important candidate loci for the major psychoses. We investigated genes with TNR polymorphisms, including B1, B33, B37, and the N-cadherin gene, in unrelated Caucasian North American and Italian schizophrenics (n = 53 to 74), and matched controls. Also, unrelated Caucasian North American patients with bipolar I affective disorder were screened for the B33 and N-cadherin genes (n = 49 and 63, respectively). No unusually long alleles that would suggest abnormal expansion of the TNR were observed for any of these genes. Also, no statistically significant results were found in tests for genetic association between any of these genes and schizophrenia. For B37, a trend toward a difference in allele counts between schizophrenics and controls was observed. However, no clear evidence for a role of these TNR-containing genes in schizophrenia or bipolar affective disorders was found.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265274
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Psychosis and genes with trinucleotide repeat polymorphism (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 244-246 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Abnormal expansion of genes with trinucleotide repeat (TNR) polymorphism has been found in a number of neuropsychiatric disorders. These disorders and the major psychoses, schizophrenia and bipolar affective disorder, appear to share an interesting phenomenon: genetic anticipation. Because TNR expansion correlates with anticipation, these unstable DNA sites are considered important candidate loci for the major psychoses. We investigated genes with TNR polymorphisms, includingB1, B33, B37, and theN-cadherin gene, in unrelated Caucasian North American and Italian schizophrenics (n = 53 to 74), and matched controls. Also, unrelated Caucasian North American patients with bipolar I affective disorder were screened for the B33 andN-cadherin genes (n = 49 and 63, respectively). No unusually long alleles that would suggest abnormal expansion of the TNR were observed for any of these genes. Also, no statistically significant results were found in tests for genetic association between any of these genes and schizophrenia. For B37, a trend toward a difference in allele counts between schizophrenics and controls was observed. However, no clear evidence for a role of these TNR-containing genes in schizophrenia or bipolar affective disorders was found.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265274
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Genetic anticipation and breast cancer: a prospective follow‐up study (1999)
    Springer
    Breast cancer research and treatment 55 (1999), S. 21-28 
    Details
    ISSN: 1573-7217
    Keywords: age of diagnosis ; ascertainment ; breast cancer ; genetic anticipation ; prospective cohort family study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Genetic anticipation is characterized by an earlier age of disease onset, increased severity, and a greater proportion of affected individuals in succeeding generations. The discovery of trinucleotide repeat expansion (TRE) mutations as the molecular correlate of anticipation in a number of rare Mendelian neurodegenerative disorders has led to a resurgence of interest in this phenomenon. Because of the difficulties presented to traditional genetics by complex diseases, the testing for genetic anticipation coupled with TRE detection has been proposed as a strategy for expediting the identification of susceptibility genes for complex disorders. In the case of breast cancer, a number of previous studies found evidence consistent with genetic anticipation. It is known that a proportion of such families are linked to either BRCA1 or BRCA2, but no TRE mutations have been identified. It has been shown that the typical ascertainment employed in studies purporting to demonstrate genetic anticipation combined with unadjusted statistical analysis can dramatically elevate the type I error. We re‐examine the evidence for anticipation in breast cancer by applying a new statistical approach that appears to have validity in the analysis of anticipation to data ascertained from a recent follow‐up of a large prospective cohort family study of breast cancer. Using this approach, we find no statistically significant evidence for genetic anticipation in familial breast cancer. We discuss the limitations of our analysis, including the problem of adequate sample size for this new statistical test.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006151132592
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Genomic imprinting in unstable DNA diseases (1996)
    New York, NY : Wiley-Blackwell
    BioEssays 18 (1996), S. 587-590 
    Details
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Evidence for recombination suppression has been identified in linkage studies of several unstable DNA diseases. Also sex-specific changes in recombination frequency have been detected at the loci of Huntington's disease and myotonic dystrophy. It can be hypothesized that meiotic recombination is regulated by genome-wide genomic imprinting and that changes in meiotic recombination imply the presence of the genomic imprinting defect. If aberrant recombination at the locus of trinucleotide repeat expansion is verified, new theoretical and experimental opportunities will arise in studies on the role of genomic imprinting in the unstable DNA diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bies.950180710
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    Paper (German National Licenses)
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