Parkinson's and Alzheimer's Today: About Neurodegeneration and its Therapy

Preface
Contents
1 Introduction to Brain Development: Why do We Need so Many Nerve Cells?
1.1 Neurons and Glia in the Central Nervous System
1.2 What Happens During Brain Development?
1.3 Evolutionarily Old Brain Parts are Simpler in Structure than the Neocortex
1.4 What Distinguishes the Left from the Right Brain?
1.5 Brain Development in Childhood and Adolescence
1.6 The Child’s Brain is Enormously Plastic and can Still Heal
1.7 Is a Large Brain “Smarter” than a Small One?
1.8 Absolute and Relative Brain Weight
1.9 With the Second Evolutionary Leap, Our Brain Reaches its Maximum Size
1.10 Neural Stem Cells Remain Capable of Dividing for a Long Time
1.11 The Frontal Lobe is Especially Important for Higher Brain Functions
1.12 The Prefrontal Cortex Encodes Human Specific Properties
1.13 Brain Performance in Comparison
Further Reading
2 Aging and Neurodegenerative Diseases: Why do Nerve Cells Die?
2.1 The Normal Aging Process
2.1.1 Mechanisms of Cellular Aging
DNA Telomeres Determine the Number of Cell Divisions
Aging Cells Maintain a Chronic Inflammation
The Importance of Protein Homeostasis for Cellular Aging
Self-cleaning of Nerve Cells
Two Sides of a Coin: Oxygen Radicals
Endogenous Radical Scavengers Protect Our Nerve Cells
Chronic Inflammatory Processes in the Brain
2.1.2 Neuronal Cell Death
How do neurons die?
2.1.3 Blood Supply of the Aging Brain
Barrier Disorders are Not Uncommon in the Elderly
2.2 Parkinson’s Disease
2.2.1 General Pathomechanisms
The Problem with Parkinson’s Begins in the Lower Brainstem
2.2.2 Special Morphology of Affected Neurons
Special Requirements for Highly Branched Neurons
Many Amine-releasing Neurons are Constantly Active and Therefore More Easily Stressed
2.2.3 Specific Causes of Parkinson’s Disease
2.2.4 Alpha-synuclein: A Key Protein in Parkinson’s Disease
Fibrils Are More Dangerous Than Aggregates
Aggregates Are Not Only Found in Nerve Cells
2.2.5 The Prion Theory of Parkinson’s Disease
Cranial Nerves Transport Pathological Proteins into the Brain
The Difficulties of a Clear Pathogenesis of Parkinson’s Disease
2.3 Dementia and Alzheimer’s Disease
2.3.1 How Does Alzheimer’s Disease Manifest Itself?
2.3.2 General Pathomechanisms
The Amyloid Pathology
The Many Effects of Aβ Peptides
2.3.3 The Disturbed Protein Homeostasis in Alzheimer’s Disease
2.3.4 Tau Pathology
Pathological Effects of p-tau and Aβ
Episodic Memory is Already Impaired in the Early Stage of Alzheimer's
2.3.5 The Prion Theory in Alzheimer’s Disease
The Relevance of Cerebrospinal Fluid Drainage for Neurodegeneration
2.4 Inflammatory Components of Alzheimer’s and Parkinson’s Disease
2.5 Viral Infections in Neurodegenerative Diseases
Further Reading
3 Saving or Replacing Nerve Cells: Which Strategy is More Successful?
3.1 Parkinson’s Disease
3.1.1 Pharmacological Therapy
3.1.2 Surgical and physical therapy
3.1.3 Therapy with Neurotrophic Factors
3.1.4 Therapy with Antisense Oligonucleotides
3.1.5 Alpha-synuclein Aggregation Inhibitors and Specific Immunotherapy
3.1.6 Stem Cell Therapy
3.1.7 Other Causal Therapeutic Approaches
3.2 Dementia and Alzheimer’s Disease
3.2.1 Cholinergica
3.2.2 Therapy with Secretase Inhibitors
3.2.3 Therapy with Neurotrophic Factors
3.2.4 Immunotherapy
3.2.5 Stem Cell Therapy
3.2.6 Other Causal Therapeutic Approaches
3.2.7 Symptomatic Therapy
3.2.8 Which Measures Promise the most Success?
3.3 Diagnosis and Therapy of Neuronal Degeneration—quo vadis?
Further Reading
Glossary