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Neurodegenerative Diseases

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Cover of 'Neurodegenerative Diseases'

Table of Contents

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    Book Overview
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    Chapter 1 Alzheimer’s Disease: Insights from Genetic Mouse Models and Current Advances in Human IPSC-Derived Neurons
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    Chapter 2 Clinical Aspects of Alzheimer’s Disease
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    Chapter 3 Parkinson’s Disease: Basic Pathomechanisms and a Clinical Overview
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    Chapter 4 Huntington’s Disease: Pathogenic Mechanisms and Therapeutic Targets
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    Chapter 5 The Complexity of Clinical Huntington’s Disease: Developments in Molecular Genetics, Neuropathology and Neuroimaging Biomarkers
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    Chapter 6 Motoneuron Disease: Basic Science
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    Chapter 7 Motoneuron Disease: Clinical
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    Chapter 8 Multiple Sclerosis: Basic and Clinical
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    Chapter 9 Schizophrenia: Basic and Clinical
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    Chapter 10 Stroke: Basic and Clinical
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    Chapter 11 Epileptic Encephalopathies as Neurodegenerative Disorders
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    Chapter 12 Neurodegeneration and Pathology in Epilepsy: Clinical and Basic Perspectives
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    Chapter 13 Prion Diseases
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    Chapter 14 Leukodystrophy: Basic and Clinical
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    Chapter 15 Traumatic Brain Injury as a Trigger of Neurodegeneration
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    Chapter 16 Cell Death Mechanisms of Neurodegeneration
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    Chapter 17 Neuroglia: Functional Paralysis and Reactivity in Alzheimer’s Disease and Other Neurodegenerative Pathologies
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    Chapter 18 Advances in Neuroimaging for Neurodegenerative Disease
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    Chapter 19 Gene Linkage and Systems Biology
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    Chapter 20 Biomarkers in Neurodegenerative Diseases
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    Chapter 21 Erratum
Attention for Chapter 9: Schizophrenia: Basic and Clinical
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Chapter title
Schizophrenia: Basic and Clinical
Chapter number 9
Book title
Neurodegenerative Diseases
Published in
Advances in neurobiology, July 2017
DOI 10.1007/978-3-319-57193-5_9
Pubmed ID
Book ISBNs
978-3-31-957191-1, 978-3-31-957193-5
Authors

Coyle, Joseph T., Joseph T. Coyle

Abstract

Schizophrenia is a chronic severe mental disorder characterized by psychosis, cognitive impairments, and social and motivational deficits. It is associated with a progressive loss of cortical volume after onset of psychosis; nevertheless, cortical atrophy correlates with the cognitive impairments and the negative symptoms but not with the psychosis. The cortical atrophy is not primarily due to neuronal degeneration but rather to neuronal atrophy and loss of glutamatergic synapses. A downregulation of the presynaptic markers for the parvalbumin-expressing GABAergic interneurons that provide recurrent inhibition to cortical pyramidal neurons is another consistent pathologic feature. Antipsychotic drugs continue after 50 years to be the mainstay of treatment although these drugs, with the possible exception of clozapine, have negligible effects on cognition and negative symptoms. Pharmacologic challenge studies, postmortem analyses and a recent sufficiently powered genome-wide association study and copy number variant studies provide compelling evidence that NMDA receptor hypofunction is an important pathophsysiologic feature of schizophrenia. Silencing the gene encoding serine racemase, the enzyme that synthesizes the cortical-limbic NMDA receptor co-agonist, D-serine, replicates the dendritic and GABAergic pathology and cognitive deficits of schizophrenia in mice. Pharmacologic strategies to overcome NMDA receptor hypofunction hold promise of treating the disabling cognitive and negative symptoms.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 60 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 60 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 11 18%
Student > Ph. D. Student 7 12%
Researcher 5 8%
Student > Bachelor 4 7%
Student > Doctoral Student 3 5%
Other 5 8%
Unknown 25 42%
Readers by discipline Count As %
Neuroscience 7 12%
Psychology 6 10%
Medicine and Dentistry 5 8%
Social Sciences 3 5%
Nursing and Health Professions 2 3%
Other 5 8%
Unknown 32 53%