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Introduction

Huntingtonʼs disease (HD) is a devastating neurodegenerative disorder that affects movement, cognition, and behavior. While the disease is primarily caused by a genetic mutation in the huntingtin gene, growing evidence suggests that neuroinflammation plays a critical role in the pathogenesis of HD. Neuroinflammation is a complex immune response in the brain that involves the activation of microglia and astrocytes, leading to the release of inflammatory mediators.

Understanding the role of neuroinflammation in HD is crucial for developing targeted therapies that can slow down or even halt the progression of the disease. This thesis aims to investigate the mechanisms underlying neuroinflammation in HD and its contribution to disease pathology.

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 Huntingtonʼs disease
2.2 Genetics of Huntingtonʼs disease
2.3 Neuroinflammation in neurodegenerative diseases
2.4 Role of microglia in neuroinflammation
2.5 Role of astrocytes in neuroinflammation
2.6 Inflammatory mediators in neuroinflammation
2.7 Neuroinflammation in Huntingtonʼs disease
2.8 Neuroinflammatory markers in HD
2.9 Therapeutic strategies targeting neuroinflammation in HD
2.10 Gaps in current knowledge

Chapter 3: Research Methodology
3.1 Study design
3.2 Participants
3.3 Data collection
3.4 Data analysis
3.5 Ethical considerations
3.6 Statistical analysis
3.7 Research instruments
3.8 Limitations of the study

Chapter 4: Discussion of Findings
4.1 Neuroinflammatory markers in HD patients
4.2 Correlation between neuroinflammation and disease severity
4.3 Mechanisms of neuroinflammation in HD
4.4 Therapeutic implications
4.5 Future research directions
4.6 Comparison with existing literature

Chapter 5: Conclusion and Summary
5.1 Summary of findings
5.2 Implications for future research
5.3 Conclusion

Thesis Overview

Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by motor dysfunction, cognitive impairment, and psychiatric symptoms. The disease is caused by a mutation in the huntingtin gene, leading to the production of mutant huntingtin protein that aggregates in the brain. While the genetic basis of HD is well-established, the role of neuroinflammation in disease pathogenesis is still not fully understood.

Neuroinflammation is a complex process involving the activation of immune cells in the brain, such as microglia and astrocytes, leading to the release of inflammatory mediators. In the context of HD, neuroinflammation has been suggested to contribute to neuronal dysfunction and cell death, exacerbating disease progression. This thesis aims to investigate the mechanisms underlying neuroinflammation in HD and its potential as a therapeutic target.

The literature review will provide an overview of HD, the genetics of the disease, and the role of neuroinflammation in neurodegenerative disorders. It will also explore the specific mechanisms of neuroinflammation in HD, including the involvement of microglia, astrocytes, and inflammatory mediators. The review will highlight the gaps in current knowledge and potential therapeutic strategies targeting neuroinflammation in HD.

The research methodology will outline the study design, participants, data collection methods, and data analysis plan. Ethical considerations and statistical analysis will also be discussed, along with the limitations of the study. The findings section will present the results of the study, including neuroinflammatory markers in HD patients, the correlation between neuroinflammation and disease severity, and potential therapeutic implications.

The discussion of findings will interpret the results in the context of existing literature, exploring the mechanisms of neuroinflammation in HD and their implications for future research. The conclusion will summarize the key findings of the study, highlight the implications for clinical practice, and suggest directions for future research on neuroinflammation in HD.

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