Chapter 1: The multitude of therapeutic targets in neurodegenerative proteinopathies
		
			- 
				Abstract
 
			- 
				Protein Misfolding and Aggregation
 
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				Mechanism of Assembly
 
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				Prion-Like Propagation of Protein Assemblies
 
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				Propagation Routes of Pathogenic Protein Aggregates
 
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				Limiting Steps in the Propagation of Pathogenic Protein Assemblies
 
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				Therapeutic Strategies Targeting the Physiological Levels of Aggregation-Prone Proteins Involved in Neurodegeneration
 
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				Therapeutic Strategies Targeting the Misfolding and Aggregation of Proteins Involved in Neurodegeneration
 
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				Therapeutic Strategies Targeting the Accumulation of Misfolded Pathologic Protein Aggregates
 
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				Therapeutic Strategies Targeting the Cell-to-Cell Propagation of Pathogenic Protein Aggregates
 
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				Therapeutic Strategies Aimed at Restoring the Damage Pathogenic Protein Aggregates Induce
 
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				Therapeutic Strategies Targeting Misfolded Pathologic Protein Aggregate–Mediated Neuroinflammation
 
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				Limitations of the Different Therapeutic Strategies
 
			- 
				Acknowledgments
 
		
		
			Chapter 2: Synuclein misfolding as a therapeutic target
		
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				Abstract
 
			- 
				Introduction
 
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				The Conformational Landscape of α-Synuclein: the Native State
 
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				The Conformational Landscape of α-Synuclein: Misfolded Variants
 
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				Misfolding of α-Synuclein as a Therapeutic Target
 
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				Conclusions
 
		
		
			Chapter 3: Neuroinflammation as a therapeutic target in neurodegenerative diseases
		
			- 
				Abstract
 
			- 
				Introduction
 
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				Glial Cells in CNS Development, Homeostasis, and Pathology
 
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				Chronic Neuroinflammation as a Common Pathophysiological Mediator in Progressive Neurodegenerative Diseases
 
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				Therapeutic Strategies Targeting Neuroinflammation in Progressive Neurodegenerative Diseases
 
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				Future Perspectives
 
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				Conclusions
 
		
		
			Chapter 4A: Stem cells in neurodegeneration: mind the gap
		
			- 
				Abstract
 
			- 
				Introduction
 
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				Part I: Stem Cells
 
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				Part II: Stem Cells as Regenerative Therapy
 
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				Part III: Stem Cells to Model Neurodegenerative Diseases
 
		
		
			Chapter 4B: The potential of stem cells in tackling neurodegenerative diseases
		
			- 
				Abstract
 
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				Endogenous Stem Cells as a Therapeutic Target
 
		
		
			Chapter 5: Preclinical models of Alzheimer’s disease for identification and preclinical validation of therapeutic targets: from fine-tuning strategies for validated targets to new venues for therapy
		
			- 
				Abstract
 
			- 
				Introduction
 
			- 
				Conclusions
 
		
		
			Chapter 6: Parkinson’s disease
		
			- 
				Abstract
 
			- 
				Introduction
 
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				Current Treatment Approaches in Parkinson’s Disease
 
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				Drugs That are Being Evaluated Clinically for Disease Modification in PD
 
			- 
				Novel Targets for Disease-Modifying Therapies in PD
 
			- 
				Conclusions
 
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				Acknowledgments
 
		
		
			Chapter 7: Lewy body dementia
		
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				Abstract
 
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				Lewy Body Dementia
 
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				Management of LBD
 
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				Concluding Remarks
 
		
		
			Chapter 8: Frontotemporal dementia
		
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				Abstract
 
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				Overview of Frontotemporal Dementia
 
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				Disease Management
 
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				Novel Possibilities in Disease-Modifying Drug Development
 
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				Discussion: Essentials for the Development of a Disease-Modifying Therapy
 
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				Conclusions
 
		
		
			Chapter 9: From huntingtin gene to Huntington’s disease-altering strategies
		
			- 
				Abstract
 
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				Huntington’s Disease
 
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				Huntingtin Gene and Transcripts
 
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				Huntingtin Protein
 
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				HD Pathogenic Mechanisms
 
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				Molecular Strategies for HD
 
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				ASO
 
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				Genome Editing
 
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				Conclusions and Perspectives
 
			- 
				Acknowledgments
 
		
		
			Chapter 10: Amyotrophic lateral sclerosis: mechanisms and therapeutic strategies
		
			- 
				Abstract
 
			- 
				Introduction
 
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				Excitotoxicity
 
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				Hyperexcitability
 
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				Pathogenic Role of Non-Neuronal Cells
 
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				Shortage of Neurotrophic Factors
 
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				Mitochondrial Dysfunction
 
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				Axonal Defects
 
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				Altered Proteostasis and Autophagy
 
			- 
				Altered RNA Metabolism and Stress Granule Formation
 
			- 
				Hexanucleotide Repeats in C9ORF72 and Disturbances in Nucleocytoplasmic Transport
 
			- 
				Conclusions
 
			- 
				Acknowledgments