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Author: Laura Lossi
Publisher: Frontiers Media SA
ISBN: 2889451119
Category :
Languages : en
Pages : 181
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Book Description
The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.
Author: Laura Lossi
Publisher: Frontiers Media SA
ISBN: 2889451119
Category :
Languages : en
Pages : 181
Get Book Here
Book Description
The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.
Author: Brian Popko
Publisher: Springer Science & Business Media
ISBN: 146154887X
Category : Medical
Languages : en
Pages : 370
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Book Description
The number of mouse models that are available for the study of human genetic neurological disorders is large and growing rapidly. Therefore, it was difficult to select the models that were reviewed in this volume. Clearly, there are important models that are not discussed, and perhaps a volume twice this size would have been more appropriate. Moreover, the pace at which new models are being developed and analyzed is rapid. As this volume goes to press, I am sure that additional mouse genes responsible for naturally occurring neurological disorders are being discovered and that many new transgenic and mutant mouse strains are being developed. Therefore, this volume should not be viewed as a comprehensive compendium, but rather as an update of work in progress. It is exhilarating to witness the fast pace at which these models are being established as important tools in the study of basic neuroscience and neurological disorders. It will be even more exciting to see their utilization in the development and testing of therapeutic interventions for these diseases. I would like to thank each of the authors who have contributed to this volume for their time and their expertise. I would also like to thank Drs. Timothy Coetzee and Joshua Corbin for their advice in the selection of the topics covered. I am deeply indebted to Dr. Kunihiko Suzuki, who first approached me with the idea for this volume, for his guidance throughout its preparation.
Author: Anil Kumar
Publisher: Bentham Science Publishers
ISBN: 9815039695
Category : Science
Languages : en
Pages : 290
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Book Description
Animal disease models are a vital tool to study diseases and associated conditions. Studies on animal models can, in some cases, be used as a basis for modeling and understanding human diseases. Biomedical scientists face a challenge to choose the correct animal model to study disease pathology, and neurological diseases are no exception to this rule. Animal Models for Neurological Disorders covers different animal models which have been used for studying neurological disorders. 13 topical chapters have been contributed by a group of experts on the subject with an aim to cover emerging experimental models of a range of neurological diseases encountered in the clinic including Alzheimer’s disease, psychosis, Parkinson’s, Huntington’s disease, vascular dementia, schizophrenia, multiple sclerosis and brain tumors, among others. The chapters also inform readers about relevant clinical correlations in each disease model where appropriate. Animal Models for Neurological Disorders is intended for all scholarly researchers and students of biomedical sciences, pharmacology, medicine (oncology, neurology, psychiatry), pharmacy, biochemistry, and biotechnology. The organized contents of the book also serve as a quick reference point for scientists working in applied areas of neuroscience including the study of neurodegenerative diseases and cognitive dysfunction in living organisms.
Author: Dirk M. Dhossche
Publisher: Gulf Professional Publishing
ISBN: 9780123668721
Category : Medical
Languages : en
Pages : 528
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Book Description
Gamma-aminobutyric acid (GABA) was discovered in the brain in 1950 by Eugene Roberts. GABA is now considered one of the most important neurotransmitters and developmental signals. Knowledge on the complexity of GABA function is increasing exponentially. This volume covers basic research on GABA in the developing brain as it may relate to onset of autism and related developmental disorders. The evidence that dysfunction of GABA and related molecules is associated with autism is limited but expanding and seems to converge. Pertinent data are reviewed in this book and new research avenues in the basic and clinical arenas are described. The topics are of imminent interest to basic and clinical researchers as well as interested clinicians. * Discusses the neuropathology of the GABA system in autism * Presents new findings on common genetic mechanisms in Rett syndrome, Angelman syndrome, and autism * Includes information on the shared genetic risk factors between autism and major mental disorders * Foreword by Eugene Roberts
Author:
Publisher: Academic Press
ISBN: 0128135662
Category : Science
Languages : en
Pages : 452
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Book Description
Epigenetics and Psychiatric Disease, Volume 157, the latest volume in the Progress in Molecular Biology and Translational Science series, includes recent developments on a variety of topics, including the Epigenetic landscapes of the adversity-exposed brain, Chromosomal conformations and epigenomic regulation in schizophrenia, Progress in the epigenetics of depression, the epigenetics of circadian rhythms in imprinted neurodevelopmental disorders, DNA methylation mediating substance abuse, mechanisms and therapeutic opportunities, DNA methylation in animals model of psychosis, Epigenetics of early life stress, Epigenetic drugs for mood disorders, and more. Accessible to students and researchers alike, with content that appeals to a variety of readers Written by leading authorities in their respective fields of molecular biology
Author: Catherine Lambert de Rouvroit
Publisher: Springer Science & Business Media
ISBN: 3642722571
Category : Medical
Languages : en
Pages : 117
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Book Description
Only five years ago, nobody in his right mind would have consid ered publishing a book on reeler as a model for brain develop ment. Although this interesting mutation has been with us for half a century, it is fair to say that, in spite of a wave of enthusiasm in the late sixties and early seventies, generated primarily by Sidman, Caviness and colleagues, studies of reeler mice fell pro gressively out of fashion during the next two decades. All that changed almost overnight when the cloning of the reeler gene, dubbed reelin, was reported in Tom Curran's laboratory in 1995. The fact that the same gene was identified at the same time independently by two other groups using positional cloning sug gested strongly that reelin was the right candidate. Although the key experiments of transgenic rescue have not been made (and perhaps will never be), the equation "reeler is reelin" has been established beyond reasonable doubt, as alterations of the reelin gene and/or its expression have been found in at least five alleles of reeler and in the mutation Shaking Rat Kawasaki (SRK), an ortholog of reeler.
Author: Jesus Avila
Publisher: Royal Society of Chemistry
ISBN: 1849732752
Category : Science
Languages : en
Pages : 307
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Book Description
In recent years, medical developments have resulted in an increase in human life expectancy. Some developed countries now have a larger population of individuals aged over 64 than those under 14. One consequence of the ageing population is a higher incidence of certain neurodegenerative disorders. In order to prevent these, we need to learn more about them. This book provides up-to-date information on the use of transgenic mouse models in the study of neurodegenerative disorders such as Alzheimer's and Huntington's disease. By reproducing some of the pathological aspects of the diseases, these studies could reveal the mechanism for their onset or development. Some of the transgenic mice can also be used as targets for testing new compounds with the potential to prevent or combat these disorders. The editors have extensive knowledge and experience in this field and the book is aimed at undergraduates, postgraduates and academics. The chapters cover disorders including: Alzheimer's disease, Parkinson's disease, Huntington's and other CAG diseases, amyotrophic lateral sclerosis (ALS), recessive ataxias, disease caused by prions, and ischemia.
Author: Jesús Avila
Publisher: Royal Society of Chemistry
ISBN: 1849731845
Category : Medical
Languages : en
Pages : 307
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Book Description
In recent years, medical developments have resulted in an increase in human life expectancy. The editors have extensive knowledge and experience in this field and the book is aimed at undergraduates, postgraduates, and academics. The chapters cover Alzheimer's disease, Parkinson's disease, Huntington's, and other neurodegenerative disorders.
Author: S.H. Fatemi
Publisher: Springer Science & Business Media
ISBN: 0387767614
Category : Medical
Languages : en
Pages : 473
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Book Description
Reelin glycoprotein is a serine protease with important roles in embryogenesis and during adult life. This comprehensive and integrative book examines the role that reelin plays in the etiology of various neuropsychiatric disorders, including schizophrenia and autism. The book provides an unprecedented analysis of this emerging and novel protein by examining evidence from genetic, neuroanatomic, biochemical, and behavioral studies.
