Neuroanatomy and Pathology of Sporadic Alzheimer's Disease (Advances in Anatomy, Embryology and Cell Biology Book 215)

As Indicated By Its Title, This Monograph Deals Chiefly With Morphologically Recognizable Deviations From The Normal Anatomical Condition Of The Human Cns. The Ad-associated Pathology Is Illustrated From Its Beginnings (sometimes Even In Childhood) To Its Final Form, Which Is Reached Late In Life. The Ad Process Commences Much Earlier Than The Clinically Recognizable Phase Of The Disorder, And Its Timeline Includes An Extended Preclinical Phase. The Further The Pendulum Swings Away From The Symptomatic Final Stages Towards The Early Pathology, The More Obvious The Lesions Become, Although From A Standpoint Of Severity They Are More Unremarkable And Thus Frequently Overlooked During Routine Neuropathological Assessment. For This Reason, The Authors Deal With The Hallmark Lesions In The Early Phases Of The Ad Process In Considerable Detail. Basic Organization Of Non-thalamic Nuclei With Diffuse Cortical Projections -- Microtubules And The Protein Tau -- Early Presymptomatic Stages -- Basic Organization Of Territories That Become Sequentially Involved After Initial Involvement Of Brainstem Nuclei With Diffuse Projections -- The Pattern Of Cortical Lesions In Preclinical Stages -- Alzheimer-associated Pathology In The Extracellular Space -- The Pattern Of Lesions During The Transition To The Symptomatic Phase And In Fully Developed Alzheimer's Disease -- Final Considerations -- Technical Addendum. Heiko Braak, Kelly Del Tredici. Includes Bibliographical References. Mode Of Access: World Wide Web. Front Matter....Pages i-xi Prologue....Pages 1-2 Introduction....Pages 3-14 Basic Organization of Non-thalamic Nuclei with Diffuse Cortical Projections....Pages 15-19 Microtubules and the Protein Tau....Pages 21-24 Early Presymptomatic Stages....Pages 25-36 Basic Organization of Territories That Become Sequentially Involved After Initial Involvement of Brainstem Nuclei with Diffuse Projections....Pages 37-55 The Pattern of Cortical Lesions in Preclinical Stages....Pages 57-73 Alzheimer-Associated Pathology in the Extracellular Space....Pages 75-93 The Pattern of Lesions During the Transition to the Symptomatic Phase and in Fully Developed Alzheimer’s Disease....Pages 95-130 Final Considerations....Pages 131-133 Technical Addendum....Pages 135-139 Back Matter....Pages 141-162 Preface; Contents; Chapter 1: Prologue; Chapter 2: Introduction; 2.1 Sporadic AD Is a Proteinopathy Linked to the Development of Intraneuronal Inclusions of Abnormal Tau Protein Which, in Lat ... ; 2.2 Some Neuronal Types Exhibit a Particular Inclination to the Pathological Process While Others Show a Considerable Resistan ... ; 2.3 Consistent Changes in the Regional Distribution Pattern of Intraneuronal Inclusions Make a Staging Procedure Possible; Chapter 3: Basic Organization of Non-thalamic Nuclei with Diffuse Cortical Projections; Chapter 4: Microtubules and the Protein Tau Chapter 9: The Pattern of Lesions During the Transition to the Symptomatic Phase and in Fully Developed Alzheimers Disease9.1 NFT Stage III: Progression into the Basal Temporal Neocortex, Including Portions of the Fusiform and Lingual Gyri, Involve ... ; 9.2 Involvement of Neocortical Chandelier Cells; 9.3 Are Stages a-III Part of the AD-Associated Pathological Process?; 9.4 Basic Organization of Insular, Subgenual, and Anterior Cingulate Regions; 9.5 NFT Stage IV: Further Progression of the Lesions into Proneocortical and Neocortical Regions Governing High Order Autonomi Chapter 5: Early Presymptomatic Stages5.1 Stage a: The Appearance of Abnormal Tau in Axons of Coeruleus Projection Neurons; 5.2 Stages b and c: Pretangle and Tangle Material Develops in the Somatodendritic Compartments of Coeruleus Neurons and Simila ... ; 5.3 Survival of Involved Neurons, Loss of Neuronal Function, and Degradation of Remnants After the Death of Involved Neurons; Chapter 6: Basic Organization of Territories That Become Sequentially Involved After Initial Involvement of Brainstem Nuclei w ... ; 6.1 The Cerebral Cortex; 6.2 The Amygdala 6.3 The Entorhinal Region and the Presubiculum6.4 The Hippocampal Formation; 6.5 Cortical Gradients in Differentiation, Myelination, and Pigmentation; 6.6 Interconnecting Pathways; Chapter 7: The Pattern of Cortical Lesions in Preclinical Stages; 7.1 Stages 1a and 1b: Development of Inclusions in Axons and of Pretangle Material in Transentorhinal Pyramidal Cells; 7.2 NFT Stages I and II; 7.3 Prevalence of Stages a-II; 7.4 The Problem of Selective Vulnerability and the Potential Transmission of Pathological Changes from One Neuron to the Next 7.5 Imaging Techniques and Soluble Tau as Biomarker in the CSFChapter 8: Alzheimer-Associated Pathology in the Extracellular Space; 8.1 The Amyloid Precursor Protein and the Abnormal Protein Abeta; 8.2 Sources and Secretion of Abeta; 8.3 Transient Extracellular Abeta Deposits; 8.4 Mature Forms of Abeta Deposits and Plaque Degradation; 8.5 Phases in the Development of Abeta Deposits; 8.6 Formation of Neuritic Plaques (NPs); 8.7 Cerebral Amyloid Angiopathy; 8.8 Soluble Abeta as a Biomarker in the CSF 9.6 Macroscopically Recognizable Characteristics of Advanced AD