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| 书名： | Neuroanatomy and Pathology of Sporadic Parkinsons Disease | |
|---|---|---|
| 作者： | Clasc\xc3\x83\xc2\xa1, F.; Frotscher, M.; Frotscher, M. | |
| 出版时间： | 2008-11-27 | |
| ISBN： | 9783540798491(P-ISBN) ，9783540798507(O-ISBN) | |
| 摘要： | ||
| 摘要： | ||
书目详情：
CONTENTS1 Prologue1.1 sPD and Parkinsonism1.2 sPD Is a Proteinopathy Linked to the Development of Abnormal Intraneuronal Inclusions Lewy Pathology: Lewy Neurites, Lewy bodies, Lewy plaques)2 Morphology of Lewy Pathology2.1 The Protein α-Synuclein2.2 Protein Misfolding and Abnormal Aggregation of α-Synuclein2.3 Light Microscopic Visualization of Lewy Pathology2.3.1 Lewy Neurites2.3.2 Granular Aggregations2.3.3 Pale Bodies and Lewy Bodies2.3.4 Lewy Plaques2.4 Degradation of Lewy Pathology2.5 Lewy Pathology Can Co-occur with Pathology Related to Other Disorders3 The Evolving Distribution Pattern of Lewy Pathology Associated with sPD Renders Neuropathological Staging Possible3.1 Incidental Lewy Pathology3.2 Presymptomatic and Symptomatic Phases3.3 Vulnerable Regions are Interconnected Anatomically4 Stage 14.1 Pathology in Olfactory Structures4.2 Basic Organization of the Medullary Autonomic Region4.3 Involvement of Preganglionic Parasympathetic Projection Neurons4.4 Pathology in the Enteric Nervous System4.5 Is sPD Inducible by a Neurotropic Pathogen Akin to a Slow Virus?4.6 Involvement of Preganglionic and Postganglionic Sympathetic Projection Neurons4.7 Pathology in Lamina I of the Spinal Cord5 Stage 25.1 Involvement of the Medulla Oblongata and Pontine Tegmentum5.2 Basic Organization of the Gain Setting System5.2.1 Lower Raphe Nuclei5.2.2 Magnocellular Reticular Nuclei5.2.3 Coeruleus–Subcoeruleus Complex5.3 Potential Functional Consequences of the Lesions6 Stage 36.1 Involvement of the Mesencephalic Tegmentum and Basal Forebrain6.1.1 Central Subnucleus of the Amygdala6.1.2 Substantia Nigra and Adjoining Nuclei6.2 Basic Organization of Nonthalamic Nuclei with Diffuse Projections6.2.1 Magnocellular Nuclei of the Basal Forebrain6.2.2 Pedunculopontine Tegmental Nucleus6.2.3 Tuberomamillary Nucleus6.2.4 Upper Raphe Nuclei6.3 Potential Functional Consequences of the Lesions7 Stage 47.1 Involvement of the Amygdala and Thalamus7.1.1 Amygdala7.1.2 Thalamus7.2 Basic Organization of the Cerebral Cortex and Limbic Circuit7.2.1 Allocortex and Neocortex7.2.2 Mesocortex7.2.3 Limbic Circuit7.3 Involvement of the Temporal Mesocortex and Hippocampal Formation7.3.1 Temporal Mesocortex7.3.2 Hippocampal Formation7.4 Involvement of Insular, Subgenual, and Anterior Cingulate Areas7.5 Potential Functional Consequences of the Lesions8 Stages 5 and 68.1 Involvement of Neocortex and Basal Ganglia8.1.1 Neocortex8.1.2 Basal Ganglia8.2 Basic Organization of the Basal Ganglia and Striatal Circuit8.2.1 Striatum8.2.2 Pallidum8.2.3 Subthalamic Nucleus8.2.4 Claustrum8.3 Dot-Like Inclusions and Abnormally Altered Astrocytes in the Forebrain8.4 Disruption of the Striatal Circuit8.5 Potential Functional Consequences of Lesions8.6 Pathologically Changed Components of the Cerebellar Circuit9 The Progression of the Cortical Lesions Mimics the Pattern of Myelination in Reverse Order10 The Staging Hypothesis: Assumptions, Challenges, Potential
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