Advances in Anatomy, Embryology and Cell Biology
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 5: Early Presymptomatic Stages
5.1 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...
6.3 The Entorhinal Region and the Presubiculum
6.4 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
7.3 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 CSF
Chapter 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
Chapter 9: The Pattern of Lesions During the Transition to the Symptomatic Phase and in Fully Developed Alzheimer´s Disease
9.1 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...
9.6 Macroscopically Recognizable Characteristics of Advanced AD
9.7 NFT Stage V: Fan-Like Progression of the Neocortical Pathology into Frontal, Superolateral, and Occipital Directions and i...
9.8 NFT Stage VI: The Pathological Process Progresses Through Premotor and First Order Sensory Association Areas into the Prim...
9.9 The Pattern of the Cortical Tau Pathology in AD Mimics the Developmental Sequence of Cortical Lipofuscin Deposits and, in ...
9.10 The Prevalence of Tau Stages and Abeta Phases in Various Age Categories and Potential Functional Consequences of the Lesi...
Chapter 10: Final Considerations
Chapter 11: Technical Addendum
11.1 Stock Solution for Physical Developer
11.2 Campbell-Switzer Technique for Brain-Amyloid Deposits
11.3 Gallyas Technique for Neurofibrillary Pathology
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