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Introduction:

Parkinsonʼs disease is a progressive neurodegenerative disorder characterized by motor symptoms such as tremors, rigidity, and bradykinesia, as well as non-motor symptoms including cognitive impairment, autonomic dysfunction, and psychiatric disturbances. While the exact etiology of the disease is still not fully understood, evidence suggests that the death of dopaminergic neurons in the substantia nigra pars compacta is a central feature of Parkinsonʼs disease pathogenesis. Understanding the mechanisms underlying neuronal death in Parkinsonʼs disease is crucial for the development of effective therapeutic strategies to slow or halt disease progression.

Table of Contents:

Chapter 1: Introduction
1.1 Introduction
1.2 Background of study
1.3 Problem Statement
1.4 Objective of study
1.5 Limitation of study
1.6 Scope of study
1.7 Significance of study
1.8 Structure of the Thesis
1.9 Definition of terms

Chapter 2: Literature Review
2.1 Overview of Parkinsonʼs disease
2.2 Pathophysiology of Parkinsonʼs disease
2.3 Role of genetics in Parkinsonʼs disease
2.4 Inflammation and immune response in Parkinsonʼs disease
2.5 Mitochondrial dysfunction in Parkinsonʼs disease
2.6 Oxidative stress and neuronal death
2.7 Protein aggregation and neurodegeneration
2.8 Autophagy and lysosomal dysfunction
2.9 Excitotoxicity and neuronal death
2.10 Neuroinflammation and neurodegeneration

Chapter 3: Research Methodology
3.1 Study design
3.2 Sampling methods
3.3 Data collection techniques
3.4 Data analysis
3.5 Ethical considerations
3.6 Statistical analysis
3.7 Validation of findings
3.8 Limitations of the study

Chapter 4: Discussion of Findings
4.1 Mechanisms of dopaminergic neuronal death in Parkinsonʼs disease
4.2 Implications for therapeutic interventions
4.3 Future research directions

Chapter 5: Conclusion and Summary
5.1 Summary of key findings
5.2 Implications for clinical practice
5.3 Recommendations for future research
5.4 Conclusion

Thesis Overview:

Parkinsonʼs disease is a multifactorial disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. The mechanisms underlying neuronal death in Parkinsonʼs disease are complex and involve a combination of genetic, environmental, and cellular factors. This thesis aims to provide a comprehensive overview of the mechanisms of neuronal death in Parkinsonʼs disease, with a focus on the role of inflammation, oxidative stress, protein aggregation, mitochondrial dysfunction, and excitotoxicity in disease pathogenesis. By elucidating the molecular pathways involved in neuronal death, this research will contribute to the development of novel therapeutic strategies for the treatment of Parkinsonʼs disease.

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