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Cellular and Molecular Events of Ischemic Brain Damage

Cellular and Molecular Events of Ischemic Brain Damage

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Reference ID: PS-23589-TM

DEDICATION

This research work titled "Cellular and Molecular Events of Ischemic Brain Damage" is dedicated to God for his enabling grace and to all computer enthusiasts who help to make life a pleasant experience.

ACKNOWLEDGEMENT

I owe my indebtedness to my Supervisor (Name of your Supervisor), the Head of Department (Name of your HOD), the Lecturers in the department of Biochemistry, Book Authors and Profound Scholars of existing/related research material for your moral support that facilitated the successful completion of my (Tertiary Institution level). I am grateful to God Almighty and my parent for their financial support in my career. I really appreciate you all for everything, Thank you very much.

TABLE OF CONTENTS

PRELIMINARY PAGES


CHAPTER ONE

INTRODUCTION


CHAPTER TWO

LITERATURE REVIEW

  • 2.1 Introduction

CHAPTER THREE

MATERIALS AND METHODS

  • 3.1 Introduction

CHAPTER FOUR

RESULTS AND DISCUSSION

  • 4.1 Introduction
  • 4.2 Results
  • 4.3 Discussion of Findings

CHAPTER FIVE

SUMMARY, CONCLUSION AND RECOMMENDATION

  • 5.1 Introduction
  • 5.2 Summary
  • 5.3 Conclusion
  • 5.4 Recommendation

REFERENCES

ABSTRACT

Brain ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. The aim of the study is to determine the Cellular and Molecular Events of Ischemic Brain Damage. In achieving this aim, the following specific objectives were laid out to examine the Cellular Events of Ischemic Brain Damage, assess the causes of Ischemic Brain Damage, identify the etiology of cerebral ischemia, develop clinically effective neuro-protective strategies for Ischemic Brain Damage related to the inattention to white matter injury, and describe the appropriate evaluation for a patient with suspected cerebral iscemia. Data were sources from textbooks, journals, newspapers and the internet were employed. This study will be of immense benefit to students and researchers who intend to know more on this study and can also be used by non-researchers to build more on their research work. This study contributes to knowledge and could serve as a guide for other study.


Cellular and Molecular Events of Ischemic Brain Damage

CHAPTER ONE

1.1 Introduction

Brain ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand (Sullivan, 2021). This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke (Ischemia, 2003). It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage (Vespa, 2005).

As a prelude to other parts of this study, this chapter will discuss the background upon which this study was initiated, the statement of problems that led to this study, the Aim and Objectives of the study. Others are Significance of the study, Scope of work, Limitations of the Study and Definition of technical terms.


1.2 Background of Study

Cerebral ischemia can be global or focal. Global cerebral ischemia is a result of systemic processes, often shock. The most common cause of global brain ischemia is systemic hypotension. Transient cerebral hypoperfusion can occur when autonomic and neurohormonal mechanisms that control blood pressure and heart rate are disrupted, as in vasovagal syncope and postural tachycardia syndromes. Structural and functional heart problems, mostly arrhythmias, are the second most frequent cause of transient global brain ischemia. When the effect is transient, the condition often manifests as a presyncope or syncope. Prolonged global ischemia, on the other hand, can result in permanent neurological injury (Li, 2020).

Brain depends upon oxidative phosphorylation for energy. It is sensitive to disturbances in oxygen and glucose supply. Following focal ischemia there is a profound deprivation of oxygen and glucose. Oxidative stress is linked to excitotoxicity, energy loss, and ionic imbalances and all these events contribute to tissue damage (Researchgate, 2021). Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis (Raichle, 1983). There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms of brain ischemia involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage (Hossmann, 1974). In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered (Raichle et al., 2009). Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible (Beers et al., 2003).

Therefore, in Nigeria where the research was carried out, the activities that was conducted is to know the Cellular and Molecular Events of Ischemic Brain Damage.


1.3 Statement of Problems

Investigation reveals that Ischemic Brain Damage results in death and dysfunction of brain cells. However, not all brain cells die immediately after an ischemic stroke. Ischemic penumbra is a perilesional area surrounding the ischemic core. Cell death occurs by a necrotic pathway characterized by ischemic or edematous cell changes, by an apoptotic pathway with a number of morphological, biochemical, pharmacological, and molecular characteristics, or by autophagocytosis. Brain depends upon oxidative phosphorylation for energy. It is sensitive to disturbances in oxygen and glucose supply. Following focal ischemia there is a profound deprivation of oxygen and glucose. Oxidative stress is linked to excitotoxicity, energy loss, and ionic imbalances and all these events contribute to tissue damage. In addition to reactive free oxygen species, nitrosative stress contributes to tissue damage. Early after the onset of ischemia, the expression of proinflammatory genes is triggered. Loss of membrane integrity, cell swelling, and organelle failure are the features of cell death following brain ischemia. The chapter discusses the stroke-induced endogenous neuroprotection.


1.4 Aim and Objectives of Study

The aim of the study is to determine the Cellular and Molecular Events of Ischemic Brain Damage. In achieving this aim, the following specific objectives were laid out as follows:

  1. To examine the Cellular Events of Ischemic Brain Damage
  2. To assess the causes of Ischemic Brain Damage
  3. To identify the etiology of cerebral ischemia.
  4. To develop clinically effective neuroprotective strategies for Ischemic Brain Damage related to the inattention to white matter injury.
  5. To describe the appropriate evaluation for a patient with suspected cerebral iscemia.

1.5 Significance of Study

This study will be of immense benefit to students and researchers who intend to know more on this study and can also be used by non-researchers to build more on their research work. This study contributes to knowledge and could serve as a guide for other study.


1.6 Scope of Study

The study focuses on the determination of Cellular and Molecular Events of Ischemic Brain Damage in Nigeria.


1.7 Limitations of the Study

During the course of this study, many things militated against its completion, some of which are:

  1. Time Constraint: The time frame given to accomplish this project was very short due to school academic calendar and it was carried out under pressure which made the researcher not to implement some necessary features.
  2. Research material: availability of research material is a major setback to the scope of the study.
  3. Frequent power failure: This made the researcher append more money on fuel to ensure sustainable power.
  4. Financial Constraint: Insufficient fund tends to impede the efficiency of the researcher in sourcing for the relevant materials, literature or information and in the process of data collection (internet).

CHAPTER TWO

2.0 Literature Review

2.1 Introduction

This chapter focuses on the review of related literature. A literature review includes the current knowledge as well as theoretical and methodological contributions to a particular topic. It documents the state of the art with respect to the topic you are writing. It surveys the literature in the topic selected. In this research work the literature review includes the …

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