Alzheimer’s disease (AD) has been defined as a type of dementia that causes problems with memory, thinking, and behavior. AD is characterized by tau tangles and Aβ plaques in and around neurons, respectively. The impact this disease has on its victims’ health, both physically and mentally, is unimaginable and the rate of progression is not expected to decrease any time soon. This threat to our minds encourages the importance of understanding AD. Amongst the theories as to what bio mechanisms cause the brain to intertwine is the amyloid cascade hypothesis. The purpose of this thesis is to review the amyloid cascade hypothesis and discuss treatments which utilize this model. We also wish to examine social aspects such as loneliness and socioeconomic factors which are associated with the progression of AD. Research presented provides evidence that targeting the accumulation of Aβ in the brain will prevent further biochemical responses to form neurodegenerative pathology. From the collected data, we observe that therapies targeting the amyloidogenic pathway have received positive feedback in the medical community. Amongst them, an Aβ synthetic peptide vaccine which made history in vaccine development due to their responder rate. The impact of social factors such as loneliness in the advancement of AD is also supported by research. While it is acknowledged that any neurodegenerative disease is far too complex to narrow its cause specifically, this thesis provides an association with multiple aspects that can be understood and applied to future research in this field. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2018. / FAU Electronic Theses and Dissertations Collection

by Ma Suk Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 106-129). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Publications --- p.vi / Abbreviations --- p.vii / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1 --- Epidemiology of AD --- p.2 / Chapter 1.2 --- Clinical and pathological features of AD --- p.3 / Chapter 1.2.1 --- Clinical features of AD --- p.3 / Chapter 1.2.2. --- Pathological features of AD --- p.3 / Chapter 1.3 --- Diagnosis of AD --- p.4 / Chapter 1.4 --- Classification of AD --- p.5 / Chapter 1.5 --- Causes of AD --- p.5 / Chapter 1.6 --- Risk factors --- p.5 / Chapter 1.6.1 --- Age --- p.5 / Chapter 1.6.2 --- Family history --- p.6 / Chapter 1.6.3 --- Genetics --- p.6 / Chapter 1.6.3.1 --- Autosomal dominant mutations --- p.6 / Chapter 1.6.3.2 --- Genotypes of Apolipoprotein E --- p.6 / Chapter 1.6.4 --- Environmental factors --- p.7 / Chapter Chapter 2 --- Pathology in Alzheimer's disease --- p.8 / Chapter 2.1 --- Overview of Alzheimer's disease pathology --- p.8 / Chapter 2.2 --- Amyloid plaques --- p.8 / Chapter 2.2.1 --- Amyloid precursor protein --- p.8 / Chapter 2.2.2 --- Processing ofAPP --- p.9 / Chapter 2.2.3 --- Amyloid β (Aβ) --- p.12 / Chapter 2.2.4 --- APP mutations and AD --- p.12 / Chapter 2.3 --- Neurofibrillary tangles (NFT) --- p.15 / Chapter 2.3.1 --- Tau --- p.15 / Chapter 2.3.2 --- Tau mutation and neurodegeneration --- p.17 / Chapter 2.4 --- Hypotheses for AD pathology --- p.18 / Chapter 2.4.1 --- Amyloid cascade hypothesis --- p.18 / Chapter 2.4.2 --- Inflammatory hypothesis --- p.20 / Chapter 2.4.2.1 --- Microglia and astrocytes --- p.21 / Chapter 2.4.2.2 --- Inflammatory cytokines --- p.23 / Chapter 2.4.2.3 --- Inflammation and AD --- p.25 / Chapter 2.4.3 --- ApoE hypothesis --- p.27 / Chapter 2.4.3.1 --- Apolipoprotein E --- p.27 / Chapter 2.4.3.2 --- ApoE and AD --- p.28 / Chapter 2.5 --- Theory towards the pathology of AD --- p.30 / Chapter Chapter 3 --- ApoE genotyping --- p.32 / Chapter 3.1 --- Introduction --- p.32 / Chapter 3.2 --- Materials and methods --- p.32 / Chapter 3.2.1 --- Patients and control subjects --- p.32 / Chapter 3.2.2 --- Blood sampling --- p.33 / Chapter 3.2.3 --- DNA genotyping --- p.34 / Chapter 3.2.4 --- Statistical analysis --- p.35 / Chapter 3.3 --- Results --- p.35 / Chapter 3.. --- Discussion --- p.38 / Chapter Chapter 4 --- IL-1β polymorphism in relation to the risk of ADin Chinese --- p.39 / Chapter 4.1 --- Introduction --- p.39 / Chapter 4.2 --- Materials and methods --- p.44 / Chapter 4.2.1 --- Patients and control subjects --- p.44 / Chapter 4.2.2 --- Blood sampling --- p.44 / Chapter 4.2.3 --- DNA genotyping --- p.44 / Chapter 4.2.4 --- Statistical analysis --- p.48 / Chapter 4.3 --- Results --- p.48 / Chapter 4.4 --- Discussion --- p.53 / Chapter Chapter 5 --- TNFα polymorphism in relation to the risk of ADin Chinese --- p.63 / Chapter 5.1 --- Introduction --- p.63 / Chapter 5.2 --- Materials and methods --- p.66 / Chapter 5.2.1 --- Patients and control subjects --- p.66 / Chapter 5.2.2 --- Blood sampling --- p.66 / Chapter 5.2.3 --- DNA genotyping --- p.66 / Chapter 5.2.4 --- Haplotype determination --- p.70 / Chapter 5.2.5 --- Statistical analysis --- p.70 / Chapter 5.3 --- Results --- p.70 / Chapter 5.4 --- Discussion --- p.75 / Chapter Chapter 6 --- LRP8 polymorphism in relation to the risk of ADin Chinese --- p.81 / Chapter 6.1 --- Introduction --- p.81 / Chapter 6.2 --- Materials and methods --- p.87 / Chapter 6.2.1 --- Patients and control subjects --- p.87 / Chapter 6.2.2 --- Blood sampling --- p.87 / Chapter 6.2.3 --- DNA genotyping --- p.87 / Chapter 6.2.4 --- Statistical analysis --- p.89 / Chapter 6.3 --- Results --- p.91 / Chapter 6.4 --- Discussion --- p.98 / Chapter Chapter 7 --- Conclusions and prospects for future work --- p.102 / Chapter 7.1 --- Conclusion --- p.102 / Chapter 7.2 --- Prospects for future work --- p.105 / Reference --- p.106