The molecular and clinical pathology of neurodegenerative disease /
The Molecular and Clinical Pathology of Neurodegenerative Disease brings together in one volume our current understanding of the molecular basis of neurodegeneration in humans, targeted at neuroscientists and graduate students in neuroscience, and the biomedical and biological sciences. Bringing tog...
Clasificación: | Libro Electrónico |
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Autores principales: | , |
Formato: | Electrónico eBook |
Idioma: | Inglés |
Publicado: |
London :
Academic Press,
[2018]
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Temas: | |
Acceso en línea: | Texto completo |
Tabla de Contenidos:
- Front Cover; The Molecular and Clinical Pathology of Neurodegenerative Disease; The Molecular and Clinical Pathology of Neurodegenerative Disease; Copyright; Contents; Preface; Acknowledgments; 1
- AN INTRODUCTION TO NEURODEGENERATION; 1.1 WHAT IS NEURODEGENERATION?; 1.2 HOW TO USE THIS TEXTBOOK; 1.3 THE FUNDAMENTALS OF NEUROANATOMY; 1.4 A BEGINNER'S GUIDE TO BRAIN CELLS; 1.5 CLINICAL TOOLS; 1.6 METHODS AND MODELS FOR INVESTIGATING NEURODEGENERATION; 1.7 DRUGS, DRUG DEVELOPMENT, AND CLINICAL TRIALS; 1.8 SUMMARY; FURTHER READING; REFERENCES; 2
- ALZHEIMER'S DISEASE AND DEMENTIA
- 2.1 INTRODUCTION2.2 CLINICAL PRESENTATION; 2.2.1 ALZHEIMER'S DISEASE; 2.2.2 VASCULAR DEMENTIA; 2.2.3 POSTERIOR CORTICAL ATROPHY; 2.2.4 LOGOPENIC APHASIA; 2.2.5 DYSEXECUTIVE OR FRONTAL VARIANT; 2.2.6 DIAGNOSIS OF ALZHEIMER'S DISEASE; 2.2.7 MANAGEMENT; 2.2.8 FRONTOTEMPORAL DEMENTIA; 2.2.9 BEHAVIORAL VARIANT FRONTOTEMPORAL DEMENTIA; 2.2.10 LANGUAGE VARIANT; 2.2.11 DOWN SYNDROME AND TRISOMY 21; 2.2.12 DEMENTIA WITH LEWY BODIES; 2.2.13 CHRONIC TRAUMATIC ENCEPHALOPATHY; 2.2.14 OTHER DEMENTIA SYNDROMES; 2.3 PATHOLOGY; 2.3.1 NEURONAL LOSS; 2.3.2 AMYLOID PLAQUES AND NEUROFIBRILLARY TANGLES
- 2.3.3 LEWY BODIES2.3.4 GLIAL PATHOLOGY; 2.3.5 TAUOPATHIES; 2.3.6 OTHER PATHOLOGIES; 2.4 MOLECULAR MECHANISMS OF DEGENERATION; 2.4.1 NEUROGENETICS; 2.4.1.1 Mendelian Forms of Alzheimer's-APP, PSEN1, PSEN2; 2.4.1.2 Other Mendelian Genes; 2.4.1.3 Risk Factors; 2.4.2 ANIMAL AND CELLULAR MODELS FOR DISEASE; 2.4.3 PROTEIN AGGREGATION AND DISEASE; 2.4.4 THE AMYLOID CASCADE; 2.4.5 MOLECULAR MECHANISMS DRIVING NEURODEGENERATION; 2.4.6 PROTEIN AGGREGATE SPREAD; 2.4.7 NEUROINFLAMMATION AND IMMUNE RESPONSE; 2.4.8 INTERPLAY BETWEEN GENETICS, PATHOLOGY, AGING, AND SPORADIC DISEASE; 2.5 THERAPIES
- 2.5.1 EXISTING THERAPIES2.5.2 DRUG DISCOVERY; 2.5.2.1 Targeting Amyloid Beta Production; 2.5.2.2 Removing Amyloid Beta; 2.5.3 TARGETING TAU; 2.5.4 INTERVENING IN NEUROINFLAMMATION AND THE IMMUNE RESPONSE; 2.5.5 OTHER STRATEGIES; 2.5.6 WHY ARE DRUGS FAILING?; 2.6 CONCLUSIONS; REFERENCES; 3
- PARKINSON'S DISEASE; 3.1 INTRODUCTION; 3.2 CLINICAL PRESENTATION; 3.2.1 MOTOR SYMPTOMS; 3.2.2 NONMOTOR SYMPTOMS; 3.2.2.1 Neuropsychiatric; 3.2.2.2 Autonomic; 3.2.2.3 Sleep Disturbance; 3.2.2.4 Sensory; 3.2.2.5 Anosmia; 3.2.3 DEMENTIA AND PARKINSON'S DISEASE; 3.2.4 PROGRESSION/PROGNOSIS
- 3.2.5 PROGRESSIVE SUPRANUCLEAR PALSY AND MULTIPLE SYSTEM ATROPHY3.2.5.1 Progressive Supranuclear Palsy; 3.2.5.2 Multiple System Atrophy; 3.3 PATHOLOGY; 3.3.1 NIGRAL DEGENERATION; 3.3.2 LEWY BODIES; 3.3.4 DOPAMINERGIC NETWORKS; 3.3.5 BEYOND THE SUBSTANTIA NIGRA; 3.3.6 BEYOND LEWY BODIES; 3.4 MOLECULAR MECHANISMS OF DEGENERATION; 3.4.1 GENETICS; 3.4.1.1 Protein Aggregation/Proteostasis; 3.4.1.2 Mitochondrial Dysfunction; 3.4.1.3 Inflammation; 3.4.2 ENVIRONMENTAL ROUTES TO PARKINSONISM; 3.4.2.1 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine; 3.4.2.2 Rotenone and Paraquat