Role of neuroinflammation in Huntingtonʼs disease – Complete Phd and Masters Thesis

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Introduction

Huntington’s disease is a devastating neurodegenerative disorder characterized by progressive motor dysfunction, cognitive decline, and psychiatric symptoms. Although the genetic cause of Huntington’s disease is well-established, the molecular mechanisms underlying the pathology of this disease are still not fully understood. Neuroinflammation, the inflammatory response of the central nervous system, has emerged as a key player in the pathogenesis of Huntington’s disease. In recent years, increasing evidence has pointed towards the role of neuroinflammation in the progression of neurodegeneration in Huntington’s disease.

This thesis aims to explore the role of neuroinflammation in Huntington’s disease and its potential implications for the development of novel therapeutic strategies. The following chapters will provide a comprehensive overview of the current literature on neuroinflammation in Huntington’s disease, discuss the research methodology used in this study, present the findings of the research, and conclude with a summary of the key findings and their implications for future research.

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 Huntington’s disease
2.2 Neuroinflammation in neurodegenerative diseases
2.3 Role of microglia in neuroinflammation
2.4 Inflammatory mediators in Huntington’s disease
2.5 Imaging techniques for studying neuroinflammation
2.6 Therapeutic approaches targeting neuroinflammation
2.7 Animal models of Huntington’s disease
2.8 Genetics of neuroinflammation in Huntington’s disease
2.9 Biomarkers of neuroinflammation in Huntington’s disease
2.10 Future directions in neuroinflammation research

Chapter 3: Research Methodology
3.1 Study design
3.2 Participant recruitment
3.3 Data collection
3.4 Data analysis
3.5 Statistical analysis
3.6 Ethical considerations
3.7 Validity and reliability
3.8 Research limitations

Chapter 4: Discussion of Findings
4.1 Overview of findings
4.2 Neuroinflammatory profile in Huntington’s disease
4.3 Relationship between neuroinflammation and disease progression
4.4 Implications for therapeutic interventions
4.5 Novel targets for drug development
4.6 Challenges and future directions
4.7 Comparison with existing literature
4.8 Contributions to the field

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
5.5 Limitations of the study
5.6 Final thoughts

Thesis Overview: Role of Neuroinflammation in Huntington’s Disease

Huntington’s disease (HD) is a complex neurodegenerative disorder characterized by motor dysfunction, cognitive impairment, and psychiatric symptoms. The genetic cause of HD is a CAG repeat expansion in the huntingtin gene, leading to the production of a mutant huntingtin protein that aggregates in the brain. While the genetic basis of HD is well-established, the precise molecular mechanisms underlying disease pathogenesis remain unclear.

Neuroinflammation has emerged as a key player in the pathophysiology of HD. In response to mutant huntingtin protein accumulation, microglia and astrocytes in the central nervous system become activated and release pro-inflammatory mediators, leading to chronic inflammation and neuronal damage. In recent years, there has been growing interest in the potential therapeutic targeting of neuroinflammation in HD, with the aim of slowing disease progression and improving clinical outcomes.

This thesis aims to provide a comprehensive overview of the role of neuroinflammation in HD and its potential implications for the development of novel therapeutic strategies. Through a thorough review of the existing literature, a detailed discussion of research methodology, and an in-depth analysis of the findings, this thesis seeks to contribute to our understanding of the pathogenesis of HD and identify new avenues for future research.

In conclusion, the study of neuroinflammation in HD holds great promise for advancing our knowledge of disease mechanisms and developing effective treatments. By shedding light on the complex interplay between inflammation and neurodegeneration in HD, this thesis aims to make a significant contribution to the field and ultimately improve the quality of life for individuals affected by this devastating disorder.

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