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

Zhang Jiping. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 157-179). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Lu, Jianxin. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 218-241). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Zhang Lin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 68-86). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / TABLE OF CONTENTS --- p.ii / ABBREVIATIONS --- p.v / LIST OF TABLES --- p.vi / LIST OF FIGURES --- p.vii / Chapter 1. --- ABSTRACT (ENGLISH/CHINESE) --- p.1 / Chapter 2. --- INTRODUCTION --- p.6 / Chapter 3. --- LITERATURE REVIEW --- p.9 / Chapter 3.1. --- MYOPIA IN HUMAN --- p.9 / Chapter 3.1.1. --- Different types of myopia --- p.9 / Chapter 3.1.2. --- The pathologic change of myopia --- p.10 / Chapter 3.1.3. --- The prevalence of myopia --- p.13 / Chapter 3.1.4. --- Hereditary influence in human myopia --- p.13 / Chapter 3.1.5. --- Environmental influence in human myopia --- p.15 / Chapter 3.1.6. --- Nutrition in human myopia --- p.16 / Chapter 3.1.7. --- Pharmacological agents used to prevent progression of myopia --- p.16 / Chapter 3.1.8. --- Contact lens in the prevention of progression human myopia --- p.17 / Chapter 3.2. --- ANIMAL MODELS OF EXPERIMENTAL MYOPIA --- p.19 / Chapter 3.2.1. --- Experimental myopia in monkeys --- p.19 / Chapter 3.2.2. --- Experimental myopia in three shrew --- p.21 / Chapter 3.2.3. --- Experimental myopia in marmosets and guinea pigs --- p.23 / Chapter 3.2.4. --- Experimental myopia in chicks --- p.24 / Chapter 3.2.5. --- Summary --- p.26 / Chapter 3.3. --- PHARMACOLOGICAL STUDIES --- p.27 / Chapter 4. --- OBJECTIVES --- p.32 / Chapter 5. --- materials and methods --- p.34 / Chapter 5.1. --- ANIMALS AND INDUCTION OF FORM DEPRIVATION MYOPIA --- p.34 / Chapter 5.2. --- EYE GROWTH AND MYOPIC STUDY --- p.35 / Chapter 5.2.1. --- Refractive measurements --- p.35 / Chapter 5.2.2. --- Ultrasonographic measurements of eye size in vivo --- p.35 / Chapter 5.2.3. --- Measurements with calipers on enucleated eyes --- p.36 / Chapter 5.2.4. --- Weight of eye globes --- p.36 / Chapter 5.3. --- RETINAL CHANGE --- p.36 / Chapter 5.3.1. --- Light microscopy --- p.36 / Chapter 5.3.2. --- Calretinin immuno-reactivity study of the myopic retina --- p.37 / Chapter 5.4. --- DETECTION OF APOPTOTIC CELL DEATH --- p.38 / Chapter 5.4.1. --- TUNEL --- p.38 / Chapter 5.5. --- EFFECT OF RETINAL TOXINS ON MYOPIC EYES --- p.39 / Chapter 5.5.1. --- Intravitreal injection of iodoacetic acid (IAA) --- p.39 / Chapter 5.5.2. --- Intravitreal injection of glutamic acid --- p.40 / Chapter 5.5.3. --- "Intravitreal injection of 5,7-dihydrowytryptamine (5,7-DHT)" --- p.40 / Chapter 5.6. --- EFFECT OF LIGHTING ON MYOPIC EYES --- p.41 / Chapter 6. --- RESULTS --- p.42 / Chapter 6.1. --- REFRACTIVE STATES --- p.42 / Chapter 6.2. --- EYE SIZE MEASUREMENTS --- p.42 / Chapter 6.2.1. --- Ultrasonographic measurements in vivo --- p.42 / Chapter 6.2.2. --- Caliper measurements of chick eyes ex vivo --- p.43 / Chapter 6.3. --- WEIGHT OF EYE GLOBES --- p.45 / Chapter 6.4. --- RETINAL CHANGE --- p.45 / Chapter 6.4.1. --- Morphological features --- p.45 / Chapter 6.4.2. --- Morphometry of calretinin immuno-positive cells --- p.46 / Chapter 6.5. --- EFFECT OF RETINAL TOXINS ON MYOPIC EYE --- p.46 / Chapter 6.5.1. --- Intravitreal injection of iodoacetic acid (IAA) --- p.46 / Chapter 6.5.1.1. --- Eye growth measurements --- p.47 / Chapter 6.5.1.2. --- Retinal histological features --- p.47 / Chapter 6.5.2. --- Intravitreal injection of glutamic acid --- p.48 / Chapter 6.5.2.1. --- Eye growth measurements --- p.48 / Chapter 6.5.2.2. --- Retinal histological features --- p.49 / Chapter 6.5.3. --- "Intravitreal injection of 5,7,-dihydrowytryptamine (5,7-DHT)" --- p.50 / Chapter 6.5.3.1. --- Eye growth measurements --- p.50 / Chapter 6.5.3.2. --- Retinal histological features --- p.50 / Chapter 6.6. --- EFFECT OF LIGHTING ON MYOPIC EYES --- p.51 / Chapter 6.6.1. --- Eye growth measurements --- p.51 / Chapter 6.6.2. --- Retinal histological features --- p.51 / Chapter 7. --- DISCUSSION --- p.53 / Chapter 7.1. --- REFRACTIVE STATES --- p.55 / Chapter 7.2. --- CHANGE IN EYE SIZE --- p.56 / Chapter 7.2.1. --- The rate of eye growth --- p.56 / Chapter 7.2.2. --- Ultrasonographic measurements --- p.57 / Chapter 7.2.3. --- Axial length change with caliper measurements --- p.58 / Chapter 7.3. --- MORPHOLOGY AND MORPHOMETRY OF MYOPIC RETINA --- p.58 / Chapter 7.4. --- EFFECT OF RETINAL TOXINS ON MYOPIC EYES --- p.60 / Chapter 7.4.1. --- Intravitreal injection of iodoacetic acid --- p.60 / Chapter 7.4.2. --- Intravitreal injection of glutamic acid --- p.61 / Chapter 7.4.3. --- "Intravitreal injection of 5,7-DHT" --- p.63 / Chapter 7.5. --- EFFECT OF LIGHTING ON MYOPIC EYES --- p.64 / Chapter 8. --- CONCLUSION --- p.66 / BIBLIOGRAPHY --- p.68

by Chong Yin Yue. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 146-161). / Abstracts in English and Chinese. / Acknowledgments --- p.i / Abstract (English/Chinese) --- p.ii / Contents --- p.vi / List of Tables --- p.ix / List of Figures --- p.xi / Chapter I. --- INTRODUCTION --- p.1 / Chapter I.1. --- Central Nervous System Tumors --- p.1 / Chapter I.2. --- Histopathological Classification of Gliomas --- p.4 / Chapter I.2.1. --- Astrocytic Tumors --- p.4 / Chapter I.2.1.1. --- Diffuse Astrocytomas --- p.4 / Chapter I.2.1.1.1. --- Low Grade Diffuse Astrocytomas --- p.5 / Chapter I.2.1.1.2. --- Anaplastic Astrocytomas --- p.5 / Chapter I.2.1.1.3. --- Glioblastomas --- p.6 / Chapter I.2.1.2. --- Pilocytic Astrocytomas --- p.9 / Chapter I.2.1.3. --- Pleomorphic Xanthoastrocytomas --- p.10 / Chapter I.2.2. --- Non-Astrocytic Tumors --- p.10 / Chapter I.2.2.1. --- Oligodendroglial Tumors --- p.10 / Chapter I.2.2.2. --- Ependymal Tumors --- p.16 / Chapter I.2.2.3. --- Dysembryoplastic Neuroepithelial Tumors --- p.20 / Chapter I.3. --- Molecular Genetics in Gliomas --- p.21 / Chapter I.4. --- Telomeres and Telomerase --- p.29 / Chapter I.4.1. --- History --- p.29 / Chapter I.4.2. --- Telomeres --- p.30 / Chapter I.4.3. --- End Replication Problem --- p.32 / Chapter I.4.4. --- Telomerase --- p.34 / Chapter I.4.5. --- Telomerase Components --- p.36 / Chapter I.4.5.1. --- RNA Component --- p.36 / Chapter I.4.5.2. --- Protein Component --- p.39 / Chapter I.4.5.3. --- Catalytic Subunit --- p.40 / Chapter I.4.5.4. --- Telomeric Repeat Binding Factor 1 --- p.41 / Chapter I.4.6. --- Cellular Immortality and Aging --- p.42 / Chapter I.4.7. --- Detection of Telomerase Activity --- p.44 / Chapter I.4.7.1. --- Telomeric Repeat Amplification Protocol Assay --- p.44 / Chapter I.4.7.2. --- Other Detection Methods --- p.45 / Chapter I.4.8. --- An Overview of Telomerase Activity --- p.48 / Chapter I.4.9. --- Alternative Lengthening of Telomeres --- p.50 / Chapter I.4.10. --- Telomeres Suppressor Genes --- p.51 / Chapter I.4.11. --- Telomerase and pl6/pRb Pathway --- p.52 / Chapter I.5. --- Telomeres and Telomerase Studies in Brain Tumors --- p.54 / Chapter I.5.1. --- Telomerase Activity in Brain Tumors --- p.54 / Chapter I.5.2. --- Telomere Length in Brain Tumors --- p.57 / Chapter I.5.3. --- Telomerase RNA Component Expression in Brain Tumors --- p.57 / Chapter II. --- OBJECTIVES of STUDY --- p.59 / Chapter III. --- MATERIALS AND METHODS --- p.61 / Chapter III.l. --- Telomerase Activity Study --- p.61 / Chapter III.1.1. --- Specimens --- p.61 / Chapter III.l.2. --- Telomerase Extraction --- p.63 / Chapter III.1.3. --- Protein Concentration Measurement --- p.63 / Chapter III.1.4. --- RNase-treated Samples --- p.64 / Chapter III.l.5. --- TRAP Assay --- p.64 / Chapter III.1.5.1. --- TS Primer Labelling --- p.65 / Chapter III.1.5.2. --- TS Primer Extension And PCR Amplification --- p.65 / Chapter III. 1.6. --- Non-Denaturing Polyacrylamide Gel Electrophoresis --- p.66 / Chapter III.1.7. --- Data Analysis --- p.67 / Chapter III.1.8. --- Statistical Analysis --- p.67 / Chapter III.2. --- Telomere Length Study --- p.68 / Chapter III.2.1. --- Specimens --- p.68 / Chapter III.2.2. --- DNA Extraction --- p.70 / Chapter III.2.3. --- DNA Concentration Measurement --- p.71 / Chapter III.2.4. --- Analysis of Telomere Length by Southern Hybridization --- p.71 / Chapter III.2.4.1. --- DNA Digestion --- p.73 / Chapter III.2.4.2. --- Southern Blotting --- p.73 / Chapter III.2.5. --- Data Analysis --- p.76 / Chapter III.2.6. --- Statistical Analysis --- p.77 / Chapter III.3. --- hTERT and hTEP1 mRNA Expression Study --- p.78 / Chapter III.3.1. --- Specimens --- p.78 / Chapter III.3.2. --- RNA Extraction and DNase Treatment --- p.78 / Chapter III.3.3. --- Reverse Transcription-Polymerase Chain Reaction --- p.80 / Chapter III.3.3.1. --- Primer Design --- p.81 / Chapter III.3.3.2. --- Standard Protocol --- p.81 / Chapter III.3.4. --- Statistical Analysis --- p.84 / Chapter III.4. --- p16 and pRb Immunostaining --- p.85 / Chapter III.4.1. --- Specimens --- p.85 / Chapter III.4.2. --- Slide Preparation --- p.85 / Chapter III.4.3. --- Immunohistochemistry --- p.87 / Chapter III.4.4. --- Data Analysis --- p.88 / Chapter III.4.5. --- Statistical Analysis --- p.89 / Chapter IV. --- RESULTS --- p.90 / Chapter IV.1. --- Telomerase Activity Study --- p.90 / Chapter IV.2. --- Telomere Length Study --- p.96 / Chapter IV.3. --- hTERT and hTEPl mRNA Expression Study --- p.104 / Chapter IV.4. --- p16 and pRb Protein Expression --- p.109 / Chapter V. --- DISCUSSION --- p.115 / Chapter V. 1. --- Telomerase Activity in Gliomas --- p.115 / Chapter V.2. --- Telomere Length in Oligodendroglial and Ependymal Tumors --- p.122 / Chapter V.3. --- hTERT and hTEPl mRNA Expression in Oligodendroglial and Ependymal Tumors --- p.128 / Chapter V.4. --- Protein Expression ofpl6 and pRb in Oligodendroglial and Ependymal Tumors --- p.132 / Chapter V.5. --- Discussion on Telomerase Activity-Related Factors --- p.135 / Chapter V.6. --- Significance of Study and Clinical Application --- p.137 / Chapter V.7. --- Future Direction --- p.141 / Chapter VI. --- CONCLUSION --- p.143 / Chapter VII. --- REFERENCES --- p.146

by Lam Shun-Chiu Dennis. / Thesis (M.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 159-172). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

by Chan Chi Wai, Michael. / "July 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 238-272). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

by Hiu-Ming Li. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 176-198). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Michael Scott Rogers. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 265-314). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

Kok Dick Shun , Louis. / Thesis (Ph.D.)--Chinese University of Honbg Kong, 1997. / Includes bibliographical references (p. i-xiii). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.