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E-grāmata: Molecular and Clinical Pathology of Neurodegenerative Disease

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(National Hospital for Neurology and Neurosurgery, UK), (University of Reading, and UCL Institute of Neurology, UK)
  • Formāts: PDF+DRM
  • Izdošanas datums: 16-Nov-2018
  • Izdevniecība: Academic Press Inc
  • Valoda: eng
  • ISBN-13: 9780128110706
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Molecular and Clinical Pathology of Neurodegenerative DiseasePalielināt
  • Formāts: PDF+DRM
  • Izdošanas datums: 16-Nov-2018
  • Izdevniecība: Academic Press Inc
  • Valoda: eng
  • ISBN-13: 9780128110706
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The Molecular Pathology of Neurodegenerative Disease brings together the current understanding of the molecular basis of neurodegeneration in humans in a form that is targeted not only for neuroscientists, but also for graduate students in neuroscience and the biomedical and biological sciences. There are a large number of existing books covering this subject that are aimed at a clinical audience (both at undergraduate and higher level), however the increasing interest in neurodegeneration for more basic science courses – neuroscientists, biologists, pharmacists and so forth - highlight the need for a book tailored for this audience.

  • Presents an up-to-date summary on our current understanding of neurodegeneration at a molecular, cellular and tissue level
  • Includes clinical vignettes so that basic science students can relate underlying molecular processes to clinical symptoms
  • Provides background on the history of neurodegeneration
  • Highlights the state-of-the-art treatment options for each disorder
Preface xi
Acknowledgments xiii
Chapter 1 An Introduction to Neurodegeneration
1(24)
1.1 What is Neurodegeneration?
1(2)
1.2 How to Use This Textbook
3(1)
1.3 The Fundamentals of Neuroanatomy
3(3)
1.4 A Beginner's Guide to Brain Cells
6(5)
1.5 Clinical Tools
11(2)
1.6 Methods and Models for Investigating Neurodegeneration
13(5)
1.7 Drugs, Drug Development, and Clinical Trials
18(3)
1.8 Summary
21(4)
Further Reading
21(1)
References
21(4)
Chapter 2 Alzheimer's Disease and Dementia
25(58)
2.1 Introduction
26(2)
2.2 Clinical Presentation
28(5)
2.2.1 Alzheimer's Disease
28(1)
2.2.2 Vascular Dementia
29(1)
2.2.3 Posterior Cortical Atrophy
29(1)
2.2.4 Logopenic Aphasia
29(1)
2.2.5 Dysexecutive or Frontal Variant
30(1)
2.2.6 Diagnosis of Alzheimer's Disease
30(1)
2.2.7 Management
30(1)
2.2.8 Frontotemporal Dementia
31(1)
2.2.9 Behavioral Variant Frontotemporal Dementia
31(1)
2.2.10 Language Variant
31(1)
2.2.11 Down Syndrome and Trisomy 21
32(1)
2.2.12 Dementia With Lewy Bodies
32(1)
2.2.13 Chronic Traumatic Encephalopathy
32(1)
2.2.14 Other Dementia Syndromes
33(1)
2.3 Pathology
33(5)
2.3.1 Neuronal Loss
34(1)
2.3.2 Amyloid Plaques and Neurofibrillary Tangles
35(2)
2.3.3 Lewy Bodies
37(1)
2.3.4 Glial Pathology
37(1)
2.3.5 Tauopathies
37(1)
2.3.6 Other Pathologies
37(1)
2.4 Molecular Mechanisms of Degeneration
38(18)
2.4.1 Neurogenetics
38(8)
2.4.2 Animal and Cellular Models for Disease
46(1)
2.4.3 Protein Aggregation and Disease
47(4)
2.4.4 The Amyloid Cascade
51(2)
2.4.5 Molecular Mechanisms Driving Neurodegeneration
53(1)
2.4.6 Protein Aggregate Spread
54(1)
2.4.7 Neuroinflammation and Immune Response
55(1)
2.4.8 Interplay Between Genetics, Pathology, Aging, and Sporadic Disease
56(1)
2.5 Therapies
56(8)
2.5.1 Existing Therapies
56(2)
2.5.2 Drug Discovery
58(4)
2.5.3 Targeting Tau
62(1)
2.5.4 Intervening in Neuroinflammation and the Immune Response
62(1)
2.5.5 Other Strategies
63(1)
2.5.6 Why are Drugs Failing?
63(1)
2.6 Conclusions
64(19)
References
65(18)
Chapter 3 Parkinson's Disease
83(40)
3.1 Introduction
84(1)
3.2 Clinical Presentation
84(6)
3.2.1 Motor Symptoms
86(1)
3.2.2 Nonmotor Symptoms
87(2)
3.2.3 Dementia and Parkinson's Disease
89(1)
3.2.4 Progression/Prognosis
89(1)
3.2.5 Progressive Supranuclear Palsy and Multiple System Atrophy
89(1)
3.3 Pathology
90(6)
3.3.1 Nigral Degeneration
90(1)
3.3.2 Lewy Bodies
91(2)
3.3.3 Neurochemical Deficits
93(1)
3.3.4 Dopaminergic Networks
94(1)
3.3.5 Beyond the Substantia Nigra
95(1)
3.3.6 Beyond Lewy Bodies
96(1)
3.4 Molecular Mechanisms of Degeneration
96(12)
3.4.1 Genetics
97(7)
3.4.2 Environmental Routes to Parkinsonism
104(4)
3.5 Therapies
108(7)
3.5.1 Existing Treatments
108(4)
3.5.2 Experimental Therapies
112(3)
3.6 Conclusions
115(8)
Further Reading
115(1)
References
115(8)
Chapter 4 The Prion Diseases
123(34)
4.1 Introduction
123(1)
4.2 Clinical Presentation
124(4)
4.2.1 Clinical Features of Animal Prion Diseases
125(1)
4.2.2 Creutzfeldt--Jakob Disease
126(1)
4.2.3 Gerstmann-Straussler-Scheinker Syndrome
126(1)
4.2.4 Kuru
126(1)
4.2.5 Fatal Familial Insomnia
127(1)
4.2.6 Variant Creutzfeldt--Jakob Disease
127(1)
4.3 Pathology
128(1)
4.4 Molecular Mechanisms of Degeneration
128(18)
4.4.1 Kuru
129(2)
4.4.2 Slow Viruses and Other Theories
131(1)
4.4.3 The Prion Hypothesis
132(2)
4.4.4 Inherited Prion Disease
134(1)
4.4.5 Iatrogenic/Transmissible Diseases
135(1)
4.4.6 Falsifying the Hypothesis
135(1)
4.4.7 Bovine Spongiform Encephalopathy and Variant Creutzfeldt--Jakob Disease
136(2)
4.4.8 Structural and Molecular Bases of Prion Transmission
138(5)
4.4.9 Overlap With Other Protein Folding Disorders
143(3)
4.5 Therapies
146(1)
4.6 Conclusions
147(10)
Further Reading
147(1)
References
147(10)
Chapter 5 The Motor Neuron Diseases and Amyotrophic Lateral Sclerosis
157(36)
5.1 Introduction
158(2)
5.2 Clinical Presentation and Classification
160(5)
5.2.1 Epidemiology
160(2)
5.2.2 Clinical Diversity/Related Disorders
162(1)
5.2.3 Progressive Bulbar Palsy
162(1)
5.2.4 Primary Lateral Sclerosis
163(1)
5.2.5 Primary Muscular Atrophy
163(1)
5.2.6 Spinal Muscular Atrophy
163(1)
5.2.7 Overlap With Frontotemporal Dementia
163(1)
5.2.8 Treatment
164(1)
5.3 Pathology
165(2)
5.4 Molecular Mechanisms of Degeneration
167(10)
5.4.1 The Genetics of Motor Neuron Diseases
167(3)
5.4.2 Protein Aggregation and Motor Neurons
170(2)
5.4.3 Macroautophagy as a Pathway in Amyotrophic Lateral Sclerosis
172(2)
5.4.4 Prion-Like Behavior
174(1)
5.4.5 Disruption of RNA Function
174(1)
5.4.6 Intracellular Trafficking
175(1)
5.4.7 Non-cell Autonomous Degeneration
175(1)
5.4.8 Spinal Muscular Atrophy
176(1)
5.4.9 Guam and the Kii Peninsula
176(1)
5.5 Therapies
177(2)
5.5.1 Existing Disease-Modifying Therapies
177(1)
5.5.2 Symptomatic Treatments
178(1)
5.5.3 Drug Trial Failures
178(1)
5.5.4 Spinal Muscular Atrophy and Gene Therapy
178(1)
5.5.5 Experimental Therapies and Future Directions
179(1)
5.6 Conclusions
179(14)
References
180(13)
Chapter 6 Huntington's Chorea
193(28)
6.1 Introduction
193(2)
6.2 Clinical Presentation
195(2)
6.2.1 Movement Disorder
195(1)
6.2.2 Neuropsychiatric Disturbance
196(1)
6.2.3 Cognitive
196(1)
6.2.4 Diagnosis
196(1)
6.2.5 Management
196(1)
6.2.6 Treatment of Chorea
197(1)
6.2.7 Psychiatric Treatment
197(1)
6.2.8 Treatment of Cognitive Decline
197(1)
6.3 Pathology
197(1)
6.4 Molecular Mechanisms of Degeneration
198(10)
6.4.1 Genetics
199(4)
6.4.2 Polyglutamine Repeats and Protein Biology
203(2)
6.4.3 Cellular Dysfunction
205(3)
6.5 Therapies
208(2)
6.5.1 Symptomatic Treatments
208(1)
6.5.2 Preimplantation Genetic Diagnosis
208(1)
6.5.3 Experimental Treatments
208(2)
6.6 Conclusions
210(11)
Further Reading
210(1)
References
211(10)
Chapter 7 Multiple Sclerosis
221(32)
7.1 Introduction
221(1)
7.2 Clinical Presentation
222(6)
7.2.1 Epidemiology
223(2)
7.2.2 Clinical Course and Subtypes
225(1)
7.2.3 Clinical Presentation
225(2)
7.2.4 Diagnosis
227(1)
7.2.5 Outcome
228(1)
7.3 Pathology
228(2)
7.4 Molecular Mechanisms of Degeneration
230(8)
7.4.1 Chronology of Disease
231(1)
7.4.2 Genetics
232(1)
7.4.3 Environmental Causes
233(2)
7.4.4 Experimental Allergic Encephalitis
235(1)
7.4.5 Inflammation, Autoimmunity, and Neurodegeneration
236(2)
7.5 Therapies
238(3)
7.5.1 Symptomatic Management
238(1)
7.5.2 Disease-Modifying Therapies for Relapsing Remitting Multiple Sclerosis
239(1)
7.5.3 Progressive Multiple Sclerosis
240(1)
7.5.4 Experimental Treatments
240(1)
7.5.5 The Future of Drug Development for Multiple Sclerosis
241(1)
7.6 Conclusions
241(12)
Further Reading
242(1)
References
242(11)
Index 253
Dr. Lewis has been involved in research into neurodegeneration for over 15 years, investigating dementia, the prion diseases and, for the last 10 years, Parkinsons disease. He has published over 50 peer-reviewed publications in the field of neurodegeneration, and organized a number of international conferences on Parkinsons disease, with a particular focus on Leucine Rich Repeat Kinase 2 (LRRK2). With over a decade of teaching experience, he instructs on a wide range of neuroscience-related topics to both undergraduate and postgraduate students at the University of Reading and University College London. Dr. Jennifer Spillane is a neurology specialist registrar at the National Hospital for Neurology and Neurosurgery. She completed her PhD at the Institute of Neurology and has published peer-reviewed articles over a wide range of neurological topics. She has experience teaching both undergraduate and post graduate medical students.
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