The purpose of this study was to test one theoretical explanation for elders' perceived current adequacy of everyday remembering, and the antecedent perceptions, values and beliefs, and consequent feelings related to this perception. Fourteen hypotheses, deduced from the theory of subjective forgetfulness in elders (Cromwell, 1991), tested one theoretical explanation for the relationships among: Personal Importance of Remembering, Perceived Seriousness of Forgetting, Perceived Frequency of Forgetting, Belief in a Relationship between Aging and Memory Decline, Belief in a Personal Health Risk for Memory Decline, Perceived Current Adequacy of Everyday Remembering, Distress about Current Forgetting, Concern about Future Forgetting and Self Esteem in elders. Multiple regression analysis of the data obtained from 202 community based elders, age 65 to 97, supported the assertions that perceiving self to forget frequently negatively influenced elders' judgments of their current memory adequacy and increased their distress about current forgetting. Believing that one had risk factors for memory decline influenced the current distress experienced about forgetting, and the level of concern about future memory. Present concerns about forgetting, in response to perceived frequency of forgetting and perceived risks, influenced in part the degree to which the present situation was viewed as a warning sign of potential progressive future decline. Concerns about memory and forgetting influenced elders' level of self esteem. Intriguing differences in the relationships among antecedent perceptions, values and beliefs, and consequent feelings about self were discovered between older and younger elders, and between elders who highly valued remembering and those for whom remembering was of lesser importance. Future research to expand our understanding of the subjective experience of forgetfulness in elders and potential future intervention research to increase perceived memory adequacy and decrease present and future concerns were proposed.

Thirty-two parkinsonians were compared to 32 age-, sex-, and education-matched healthy controls on measures of depression (Beck Inventory), dementia (Mattis Dementia Rating Scale), and primary and secondary memory components of Free Verbal Recall. Parkinsonians were found to be more depressed, with greater impairment of secondary memory. There were no significant group differences in primary memory or general cognitive functioning. Sub-groups of 41 parkinsonians (including the 32 patients described above) were used to compare the relative contributions of depression, age of onset, and general cognitive decline to the observed secondary memory deficit. Depressed parkinsonians demonstrated more impaired primary memory than did nondepressed parkinsonians, but did not account for the difference in secondary memory. Parkinsonians with later ages of onset demonstrated greater depression and cognitive decline over a shorter length of illness, and parkinsonians with greater cognitive decline performed more poorly on the measure of secondary memory. Comparisons of parkinsonians with predominant unilateral motor symptoms (either right or left) to those with equal bilateral symptoms revealed the bilateral group to be significantly older, with later ages of onset but no difference in length of illness. It is concluded that later age of onset is a critical factor that is more likely to be associated with depression and declines in cognitive functioning than is seen with earlier age of onset. The relationship between age of onset and cognitive decline is not accounted for by age alone, length of illness, nor by the interaction of age with parkinsonian symptoms. Furthermore, the presence of bilateral symptoms may serve as a marker for the cluster of symptoms associated with later ages of symptoms onset.

This final report documents the theoretical development and preliminary empirical testing of a model that predicts the conditions under which Hispanics will seek preventive health care. Research shows that Hispanics delay preventive care, resulting in higher morbidity and mortality rates for serious diseases such as cancer. Since many serious diseases, such as heart disease, diabetes and cancer can be prevented or treated more effectively if detected early, it is crucial to understand the motivating forces behind Hispanics’ preventive health behavior. The Hispanic model, which is an extension of the Health Behavior in Cancer Prevention Model developed by Atwood, et al. (1986), includes as core variables environmental barriers to access and English-language proficiency, as well as social support, health beliefs, self-efficacy (or perceived skill), health locus of control, and health values. This correlational descriptive study employed snowballing sampling methods and consisted of 199 Hispanics between 49 and 94 years of age. Measures consist of multi-item scales whose content follows that of the Parent Project. The final instruments showed reliability (Alphas between .69 and .95), although the model testing was limited by the exclusion of some constructs that did not demonstrate reliability. The outcome of predisposition to self-care was predicted by utilization barriers to care, Chance Health Locus of Control, and General Health threat, resulting in an R-square of .07. The findings dealing with dietary preferences and preferred dietary modifications also have great implications for interventions aimed at preventing colon cancer among Hispanics. The practical health policy applications of the model are also discussed.

This study investigated quantitative and qualitative aspects of memory in three age-and-education-matched groups (1) 38 normal elderly, (2) 15 patients with dementia of the Alzheimer's type (DAT), and (3) 26 depressed elderly. Three clusters of dependent variables were used to examine group differences: (1) standard psychometric (Wechsler Memory Scale logical memory and visual reproduction subtests), (2) verbal recall measures (free recall measures of primary memory, secondary memory, prior item intrusions and extra list intrusions), and (3) verbal recognition memory measures (true positive, false positive, true negative, and false negative responses). Analyses of variance, with specified contrasts, found the DAT patients to demonstrate a pervasive memory impairment affecting both the qualitative and quantitative memory indices compared to depressed and normal elderly. The depressed elderly demonstrated impairment, compared to normal elderly, on tasks requiring effortful processing. Findings support pervasive memory loss in DAT patients and do not support clear memory impairment in the present depressed sample.

The purpose of this study was to examine the relationship between health promotion and quality of life in noninstitutionalized older adults. The study was conducted within the framework of Nola Pender's Health Promotion Model.Approval for this study was obtained from the Institutional Review Board of Ball State University for human protection of the participants. Permission from the five churches' boards was obtained. Written assurance of anonymity of subjects was given.This study was descriptive and correlational. Quality oflife was the dependent variable and the independent variables were health promoting behaviors, importance of health, perceived health status, the number of chronic health conditions and any consequent disruption to life, prior involvement in a senior citizens' wellness group or with a health advisor, and demographic variables including age, gender, marital status, living alone or with a companion or family, and education. Volunteer subjects aged 65 and older from five church groups were asked to complete the following questionnaires: Health Promoting Lifestyle Profile, Quality of Life Index, Value Survey, and a demographic sheet. The demographic questionnaire included an item regarding self-perceived health status, whether or not the participant had been involved in a wellness group or with a health advisor for older adults, and a checklist of chronic health conditions and whether or not these had had debilitating consequences for the participant.Hypotheses included the following: (1) There is no correlation between health promoting behavior and quality of life among older adults. (2) There is no correlation between importance of health and quality of life among older adults. (3) There is no correlation between perceived health status and quality of life among older adults. (4) There is no correlation between the number of chronic health conditions and quality of life among older adults. (5) There is no correlation between disruption brought about by chronic health conditions and quality of life among older adults. (6) There is no significant difference between those older adults who had participated in a senior citizens' wellness group or with a health advisor and those who had not. (7) There are no significant differences in older adult males and females and those who live alone or with family or a companion regarding quality of life. (8) There is no correlation between age and quality of life among older adults. (9) There is no correlation between number of years of education and quality of life among older adults.Statistical significance was found between Quality of Life Index and Health Promoting Lifestyle Profile scores (r=0.24, p<0.05) and Quality of Life Index and self-perceived health status scores (r=0.33, p<0.01). Other correlations, t-test, and analyis of variance did not achieve statistical significance. / School of Nursing

This thesis explores age differences in the ability to decode basic social cues from the face and, in particular, the eye region. Age-related declines in complex aspects of social perception, such as forced choice labelling of emotional expressions and theory of mind reasoning, are well documented.  However, research, to date, has not assessed age differences in more basic aspects of social perception such as eye-gaze detection, joint attention, or more implicit responses to emotional cues.  The first two experimental chapters of this thesis report a series of studies investigating age-related changes in gaze processing.  Both the ability to detect subtle differences in gaze direction and to subsequently follow the gaze cues given by others was found to decline with age. Age-related changes were also found in the integration of gaze direction with emotional (angry, joyful and disgusted) facial expressions, when making emotion perception and approachability judgements (Chapters 4 and 5).  Age differences in responses to happy facial expressions are further investigated in Chapter 6 by assessing sensitivity to discriminate between enjoyment and non-enjoyment smiles.  Findings indicated that older adults demonstrated a greater bias towards thinking that any smiling individual was feeling happy.  They were also more likely than younger participants to choose to approach an individual displaying a non-enjoyment smile.  The final experimental chapter explores whether the age of the face influences age-related changes in gaze following.  Age-related declines in gaze following were greatest when following the gaze cues of younger (vs. older) adults, highlighting the importance of closely matching age of stimulus and participant when investigating age differences in social perception.  Perceptual, neuropsychological and motivational explanations for these results are evaluated and implications of these research findings for older adults’ social functioning are discussed.

This dissertation breaks new ground. It examines the perceptions of older adults towards AIDS prevention. Using the National Health Interview Survey, 1988: AIDS Knowledge and Attitudes Supplement, a modified Health Belief Model is developed. Despite the low number of older adults 55+ with AIDS, some extenuating circumstances increase their risk of AIDS contraction. Older adults have lower levels of knowledge about AIDS, weaker immune systems and receive more blood transfusions. Societal influences include educational neglect at the hands of physicians, healthcare workers and social service personnel. The first stage of the dissertation involved establishing older adults as an at-risk population through an extensive literature review. Next, the data was described utilizing frequencies, correlations and factor analysis. Frequencies clearly indicated that older adults in the data set had low levels of AIDS knowledge and did not view themselves at risk for AIDS contraction. Correlations between the variables were minimal. A modified Health Belief Model was developed and tested. Multiple regression determined that minimal variation in the two dependent variables, "Perceived Effectiveness of Effective Methods to Prevent AIDS Contraction" and "Perceived Effectiveness of Ineffective Methods to Prevent AIDS Contraction" was accounted for by the independent variables. Although F ratios allowed rejection of the two null hypotheses, beta weights were low. Adjusted R^2's accounted for only 21% and 16% respectively of the variation in the dependent variables. Finally, discrepancies in the model were determined and recommendations made for further research. Most health belief models concentrate on individual social-psychological variables. Due to AIDS' societal consequences, it is proposed that societal providers of education: physicians, social service workers and healthcare personnel need to be included in the model. Recommendations were made for additional research into sexual behavior of older adults and exploration of available training of physicians, healthcare and social service professionals. Finally, recommendations were made to provide training and education for both professionals as well as the elderly to prevent their growth into an at-risk population.

This study aimed to understand the differences in strength or coordination of brain regions involved in processing faces in the presence of aging and/or progressing neuropathology (Alzheimer's disease). To this end, Experiment 1 evaluated age-related differences in basic face processing and the effects of familiarity in face processing. Overall, face processing in younger (22-35yrs) and older participants (63-83yrs) recruited a broadly distributed network of brain activity, but the distribution of activity varied depending on the age of the individual. The younger population utilized regions of the occipitotemporal, medial frontal and posterior parietal cortices while the older population recruited a concentrated occipitotemporal network. The younger participants were also sensitive to the type of face presented, as Novel faces were associated with greater mean BOLD activity than either the Famous or Relatives faces. Interestingly, Relatives faces were associated with greater mean B OLD activity in more regions of the brain than found in any other analysis in Exp. 1, spanning the inferior frontal, medial temporal and inferior parietal cortices. In contrast, the older adults were not sensitive to the type of face presented, which could reflect a difference in cognitive strategies used by the older population when presented with this type of face stimuli. Experiment 2 evaluated face processing, familiarity in face processing and also emphasized the interactive roles autobiographical processing and memory recency play in processing familiar faces in mature adults (MA; 45-55yrs), older adults (OA; 70-92yrs) and patients suffering from Alzheimer's disease (AD; 70-92yrs). / MA participants had greater mean BOLD activity values in more regions of the brain than observed in either of the older adult populations, spanning regions of the medial frontal, medial temporal, inferior parietal and occipital cortices. OA, in contrast, utilized a concentrated frontal and medial temporal network and AD participants had the greatest deficit in BOLD activity overall.Age-related differences in processing faces, in processing the type of face presented, in autobiographical information processing and in processing the recency of a memory were noted, as well as differences due to the deleterious effects of AD. / by Jeanna Winchester. / Thesis (Ph.D.)--Florida Atlantic University, 2009. / Includes bibliography. / Electronic reproduction. Boca Raton, Fla., 2009. Mode of access: World Wide Web.

The current study assessed whether the accuracy of children’s self-reports of events experienced differs as a function of age and how the question is asked. Additional factors like metamemory and distractibility were assessed. Primary-school students (M= 7.7 years) and middle-school students (M = 9.7 years) completed two different versions of an event frequency measure, two times, at one week intervals. In one of the measures of event frequency, no memory prompts were provided (uncued questionnaire condition), while in the other measure, recall categories for aiding recollections were provided (cued questionnaire condition). Participants’ self-reported event frequencies for the cued and uncued questionnaires were compared with trained observers’ event frequencies for the cued and uncued conditions. Older children reported event frequency more accurately than younger participants. Participants also reported events with greater accuracy with the aid of memory prompts than without, an effect that was especially strong among the younger children. Neither metamemory nor distractibility was accountable for the differences within age groups. The findings suggest that age-related improvements in accuracy of event frequency across the transition into adolescence may, in part, be due to improvements in the ability to recall and recount those events in the absence of memory cues. / Includes bibliography. / Thesis (M.A.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection

年齡相關性黃斑變性（AMD）是發展國家高齡人群中不可逆盲的首要原因。在AMD患者中，即使在改變生活模式或進行治療后，其滲出性亞型仍導致超過80% 的病例出現嚴重視力喪失及法定盲。息肉狀脈絡膜血管病變 （PCV）是一種與滲出性AMD在臨床表型上存在相同之處的黃斑病變，它的典型病變被定性為眼底血管螢光造影時出現息肉狀的病灶。近年PCV被認為是滲出性AMD亞型中的一種，因為兩者共享相同的基因成份及環境因素。然而，PCV曾經被認為是與滲出性AMD截然不同的一種疾病，由於兩者的臨床表現並不一致。另外，PCV病人相對年輕，多為亞洲人，以及對光動力治療和抗血管內皮生長因子治療存在不同的反應。一個明確的鑒別診斷可以更好的輔助臨床醫生對患有這些疾病的老年病人進行管理，然而兩者是相同還是不同的疾病種類仍是一個具爭議性的議題。 / CFH 基因和ARMS2/HTRA1位點已被全基因組相關性研究及相關的分子學研究定位為AMD候選基因。鑒於FPR1基因的協調吞噬性白細胞激活及遷移的功能，它可能是一個新的AMD候選基因。本論文評估在滲出性AMD和PCV中FPR1作為一個新的疾病基因基因的可能，獲取滲出性AMD和PCV病人中的CFH，ARMS2，HTRA1和FPR1基因檔案，同時研究在ARMS2/HTRA1位點中基因型和疾病表型的關聯性，以此從基因學方面鑑別滲出性AMD與PCV。 / 本研究在滲出性AMD，PCV病例和對照人群中使用聚合酶鏈反應和直接測序法進行ARMS2， HTRA1， CFH 和FPR1基因篩查。本研究發現滲出性AMD和PCV之間存在不同的基因型分佈，關聯模式以及基因效應值。 / 在HTRA1的多態性中，rs11200638，rs2672598, rs1049331 和 rs2293870 在滲出性AMD和PCV之間表現出鑒別性關聯 （p < 0.001）。其中rs11200638 (p = 1.48×10⁻⁴) and rs2672598 (p = 2.27×10⁻³) 在滲出性AMD病人中相互校正后仍保持各自的顯著性，但rs2672598 未能在PCV病人中保持顯著性(p = 0.20)。並且本研究發現攜帶rs11200638和 rs2672598聯合基因型AA-CC 的病人更傾向是滲出性AMD病人，與PCV相比幾率高11.7倍。 / 在ARMS2中，有11個基因多態性與滲出性AMD和PCV存在顯著性的相關。在與rs11200638校正后，rs10490924保持和滲出性AMD的顯著相關性(p = 0.011)，但PCV中未能保持(p = 0.077)。同時，元分析結果顯示ARMS2 rs10490924和HTRA1 rs11200638不同人群的PCV中的等位基因相關性是一致的。 / 在FPR1中，rs78488639與滲出性AMD (p = 0.049, 比值比 (OR) = 2.05, 95% 信賴區間（CI）: 1.014.14)和PCV (p = 0.016, OR = 2.27, 95%CI: 1.154.47)的疾病風險存在顯著的相關性。多態性rs104229的G等位基因純合子和滲出性AMD存在顯著相關(p = 0.039, OR = 2.27, 95%CI: 1.084.74)，但在PCV中未發現相關性(p = 0.24)。多態性rs2070746 AMD (p = 0.021, OR = 0.57, 95%CI: 0.35 0.91)和rs867229 (p = 0.0091, OR = 0.54, 95%CI: 0.340.86) 的雜合子基因型與滲出性AMD相關，但在PCV中未發現相關性。與此同時，本研究在上述多態性中發現滲出性AMD和PCV之間不同的基因型分佈。 / 本研究發現在滲出性AMD和PCV病人中FPR1 rs78488639和CFH rs800292存在顯著的相互作用（ORs > 4）。兩個多態性之間的相互作用提高滲出性AMD和PCV的疾病風險，而不是僅對其中之一起作用。 / ARMS2 多態性 rs10490924 (A69S, 205G>T, pAMD = 1.01×10⁻²⁹ OR = 7.91, 95% CI: 4.93 - 12.67; pPCV = 8.25×10⁻⁷, OR = 3.51, 95% CI: 1.98 - 5.03), HTRA1 多態性rs11200638 (-625G>A, pAMD = 9.88×10⁻²⁸, OR = 6.95, 95% CI: 4.37 - 11.06; pPCV = 8.02×10⁻⁶, OR = 2.82, 95%CI: 1.77 - 4.47), CFH 多態性rs800292 (V62I, 184G>A, pAMD = 9.00×10⁻⁴ , OR = 0.58, 95% CI: 0.42 0.79; pPCV = 0.011, OR = 0.66, 95% CI: 0.49 0.90) and FPR1 多態性rs78488639 (L97M, 289C>A, pAMD = 0.049, OR = 2.05, 95% CI: 1.01 - 4.14; pPCV = 0.016, OR = 2.27, 95% CI: 1.15 - 4.47)代表各自基因的最強相關性。此外，元分析揭示了在不同種族人群PCV中的等位基因相關性顯著並且一致(ORtotal = 2.14, 95% CI: 1.97 2.33, ORtotal = 2.34, 95% CI: 1.98 2.76 and ORtotal = 0.49, 95% CI: 0.44 0.56)。表型-基因型分析發現ARMS2/HTRA1 的風險基因型和較差的治療反應呈正相關性(p = 0.04)。另外，本研究在滲出性AMD中發現HTRA1 rs11200638和吸煙的聯合作用。然而，在PCV中未觀察到次聯合作用，這可能提示兩者間存在不同的疾病機制。 / 本論文提出FPR1基因是一個新的滲出性AMD和PCV候選基因，揭示了ARMS2，HTRA1，CFH和FPR1在滲出性AMD和PCV間顯著並且一致的相關性， 提供鑒別兩者的基因學證據，闡明了ARMS2/HTRA1 的風險基因型和較差的治療反應之間的相關性以及顯示了吸煙在滲出性AMD和PCV之間的不同影響。然而，由於兩者間基因關聯的趨勢一致，目前尚未能清晰界定兩者的不同。因此，要進一步明確鑒別滲出性AMD和PCV，還需要進行不同種族的複製研究，以及更重要的是，尋找特定的PCV基因以鑒別兩個不同疾病。 / Age-related macular degeneration (AMD) is the leading cause of irreversible blindness for the elderly in developed countries. Its exudative subtype accounts for more than 80% of severe visual loss or legal blindness in AMD patients regardless of modified lifestyle and therapeutic treatments. Polypoidal choroidal vasculopathy (PCV) is a macular disorder characterized by typical polypoidal lesions on fundus angiograhpy and sharing similar phenotype with exudative AMD. PCV was suggested as a distinct disease from exudative AMD based on different clinical features in ophthalmic imaging. Furthermore, PCV patients tend to be younger and more prevalent in Asian, and have different responses to photo-dynamic therapy and anti-vascular endothelial growth factor treatments, compared to exudative AMD patients. Howerver, it has also been suggested that PCV could be a subtype of exudative AMD mainly because of their common genetic and environmental factors. Therefore, genetic differentiation between exudtive AMD and PCV might assist clinicans to determine the condition. / The complement factor H (CFH) gene, and age-related maculopathy susceptibility 2 (ARMS2)/high temperature requirement factor A1 (HTRA1) locus have been mapped for AMD by genome-wide association studies (GWAS) and subsequent molecular investigations. The formyl peptide receptor 1 (FPR1) gene, which mediates trafficking and activation of phagocytic leukocytes, is related to the AMD-associated inflammatory condition. This thesis aims to evaluate FPR1 as a novel disease gene for exudative AMD and PCV, to compare the genetic profiles of ARMS2, HTRA1, CFH, and FPR1 in exudative AMD and PCV, to investigate the correlation of ARMS2/HTRA1 genotypes with disease phenotypes, and to differentiate these two disorders throught the genomic compositions. / Case-control association studies were conducted on ARMS2, HTRA1, CFH and FPR1 in exudative AMD and PCV patients of our Hong Kong Chinese cohort using polymerase chain reaction and direct sequencing. We observed different genotypic distributions (p < 0.05), association patterns and effect sizes between these two diseases. / In HTRA1 polymorphisms, rs11200638, rs2672598, rs1049331 and rs2293870 showed differential associations between exudative AMD and PCV (p < 0.001). Both rs11200638 (p = 1.48×10⁻⁴) and rs2672598 (p = 2.27×10⁻³) remained significant after adjusting for each other in exudative AMD, whereas rs2672598 was not significantly associated with PCV (p = 0.20). The joint genotype AA-CC constructed by the risk alleles of these rs11200638 and rs2672598 were prone to exudative AMD, conferring an 11.7-fold higher risk (p = 4.00×10⁻³) when compared to PCV. / In ARMS2, 11 single nucleotide polymorphisms (SNPs) showed significant associations with both exudative AMD and PCV. After adjusting for rs11200638, ARMS2 rs10490924 remained significantly associated with exudative AMD (p = 0.011), but not with PCV (p = 0.077). / In FPR1, SNP rs78488639 significantly increased the risk to exudative AMD (p = 0.049, odds ratio (OR) = 2.05, 95% confidence interval (CI): 1.014.14) and PCV (p = 0.016, OR = 2.27, 95%CI: 1.154.47). The homozygous G allele of rs1042229 was associated with exudative AMD (p = 0.039, OR = 2.27, 95%CI: 1.084.74), but not with PCV (p = 0.24). The heterozygous genotypes of rs2070746 and rs867229 were associated with exudative AMD (p = 0.021, OR = 0.57, 95%CI: 0.35 0.91; p = 0.0091, OR = 0.54, 95%CI: 0.340.86, respectively), but not with PCV. / Significant interaction was identified between FPR1 rs78488639 and CFH rs800292, with joint ORs > 4 folds for both exudative AMD and PCV. Interactions between FPR1 rs78488639 with CFH rs800292 enhance risks to both AMD and PCV, not just one of them. / Overall, the ARMS2 rs10490924 (A69S, 205G>T, pAMD = 1.01×10⁻²⁹, OR = 7.91, 95% CI: 4.93 - 12.67; pPCV = 8.25×10⁻⁷, OR = 3.51, 95% CI: 1.98 - 5.03), HTRA1 rs11200638 (-625G>A, pAMD = 9.88×10⁻²⁸, OR = 6.95, 95% CI: 4.37 - 11.06; pPCV = 8.02×10⁻⁶, OR = 2.82, 95%CI: 1.77 - 4.47), CFH rs800292 (V62I, 184G>A, pAMD = 9.00×10⁻⁴ , OR = 0.58, 95% CI: 0.42 0.79; pPCV = 0.011, OR = 0.66, 95% CI: 0.49 0.90) and FPR1 rs78488639 (L97M, 289C>A, pAMD = 0.0487, OR = 2.05, 95% CI: 1.01 - 4.14; pPCV = 0.0161, OR = 2.27, 95% CI: 1.15 - 4.47) were responsible for the strongest association in each gene. Moreover, meta-analysis revealed a consistent and significant association of the ARMS2/HTRA1 locus with PCV in different ethnic cohorts (OR{U+209C}{U+2092}{U+209C}{U+2090}{U+2097} = 2.14, 95% CI: 1.97 2.33, OR{U+209C}{U+2092}{U+209C}{U+2090}{U+2097} = 2.34, 95% CI: 1.98 2.76 and {U+209C}{U+2092}{U+209C}{U+2090}{U+2097} = 0.49, 95% CI: 0.44 0.56, respectively). The phenotype-genotype analysis implicated a positive correlation between ARMS2/HTRA1 risk genotype and a worse response to treatment (p = 0.04) in our exudative AMD patients. In addition, joint effects between cigarette smoking and HTRA1 rs11200638 was found in exudative AMD group. However, this effect was not significant in PCV group, which might implicate a different disease mechanism. / This thesis attempts to dissect the genetic profiles of exudative AMD and PCV. Results in this thesis suggest FPR1 as a novel candidate gene for exudative AMD and PCV, reveal a significant and consistent association of ARMS2, HTRA1, CFH and FPR1 with both exudative AMD and PCV, provide evidences for genetic differentiation of these two disorders, demonstrate a significant correlation between ARMS2/HTRA1 genotypes and response to treatment, and indicate different influence of smoking in exudative AMD and PCV. However, definite differentiation between exudative AMD and PCV was limited because of the same trend of associations between these two disorders. Therefore, replication studies in other enthic populations are necessary, and identification of PCV-specific genes/polymorphisms could further differentiate PCV from exudative AMD. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Liang, Xiaoying. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 124-143). / Abstract also in Chinese. / Title page --- p.i / Abstract --- p.iii / 摘要 --- p.vii / Acknowledgements --- p.xii / Table of Contents --- p.xiii / List of Figures --- p.xix / List of Tables --- p.xxi / Abbreviations --- p.xxiv / Publications --- p.xxvii / Conference Presentations --- p.xxviii / Chapter Chapter 1: --- Introduction / Chapter 1.1. --- Normal retinal architecture --- p.1 / Chapter 1.2. --- Age-related retinal changes --- p.3 / Chapter 1.3. --- Age-related macular degeneration (AMD) --- p.7 / Chapter 1.3.1. --- Classification, clinical manifestation and disease course --- p.7 / Chapter 1.3.2. --- Exudative AMD and therapeutic strategies --- p.9 / Chapter 1.3.3. --- Pathology of AMD --- p.10 / Chapter 1.3.4. --- Risk factors and associated pathogenesis --- p.12 / Chapter 1.3.4.1. --- Age --- p.12 / Chapter 1.3.4.2. --- Ethnicity --- p.13 / Chapter 1.3.4.3. --- Oxidative stress --- p.13 / Chapter 1.3.4.3.1. --- Reactive oxygen species and AMD --- p.14 / Chapter 1.3.4.3.2. --- Antioxidants --- p.15 / Chapter 1.3.4.3.3. --- Association of oxidation genes with AMD --- p.16 / Chapter 1.3.4.4. --- Inflammation --- p.16 / Chapter 1.3.4.4.1. --- Complement in AMD --- p.17 / Chapter 1.3.4.4.2. --- The potential role of formyl peptide receptor 1 (FPR1) in AMD --- p.19 / Chapter 1.3.4.5. --- Genetic predisposition --- p.19 / Chapter 1.3.4.5.1. --- Complement factor H --- p.21 / Chapter 1.3.4.5.2. --- The 10q26 locus --- p.22 / Chapter 1.3.4.5.3. --- Phenotype-genotype correlation --- p.23 / Chapter 1.4. --- Comparisons between exudative AMD and Polypoidal choroidal vasculopathy --- p.24 / Chapter 1.4.1. --- History --- p.25 / Chapter 1.4.2. --- Natural course --- p.26 / Chapter 1.4.3. --- Epidemiological factors --- p.27 / Chapter 1.4.3.1. --- Ethnicity --- p.27 / Chapter 1.4.3.2. --- Gender --- p.27 / Chapter 1.4.3.3. --- Age --- p.28 / Chapter 1.4.3.4. --- Risk factors --- p.28 / Chapter 1.4.4. --- Clinical manifestation and histopathological features --- p.29 / Chapter 1.4.5. --- Genetic determinants --- p.29 / Chapter 1.4.5.1. --- Genes with common associations --- p.30 / Chapter 1.4.5.2. --- Genes not have common association --- p.32 / Chapter 1.4.6. --- Response to treatments --- p.32 / Chapter 1.5. --- Objectives and research prospects --- p.33 / Chapter Chapter 2: --- Materials and Methods / Chapter 2.1. --- Polymorphism identification in ARMS2, HTRA1, FPR1 and CFH --- p.39 / Chapter 2.1.1. --- Study subjects --- p.39 / Chapter 2.1.1.1. --- Diagnostic features of AMD and PCV --- p.39 / Chapter 2.1.1.2. --- Control subjects --- p.40 / Chapter 2.1.2. --- Laboratory methods --- p.40 / Chapter 2.1.2.1. --- DNA extraction and quantification --- p.40 / Chapter 2.1.2.2. --- Genotyping --- p.41 / Chapter 2.1.2.2.1. --- Polymerase chain reaction (PCR) and agrose gel electrophoresis --- p.41 / Chapter 2.1.2.2.2. --- DNA sequencing --- p.42 / Chapter 2.1.3. --- Statistical analysis --- p.43 / Chapter 2.1.3.1. --- Genotypic association analysis --- p.43 / Chapter 2.1.3.2. --- Haplotype association analysis --- p.43 / Chapter 2.1.3.3. --- Logistic regression analysis --- p.44 / Chapter 2.1.3.4. --- Joint effect analysis --- p.44 / Chapter 2.1.3.5. --- Meta-analysis --- p.45 / Chapter 2.1.3.6. --- Statistical power calculation and sample size --- p.45 / Chapter 2.2. --- Phenotype-genotype correlation in ARMS2/HTRA1 locus --- p.46 / Chapter 2.2.1. --- Patient recruitment --- p.46 / Chapter 2.2.2. --- Genotyping --- p.46 / Chapter 2.2.3. --- Outcome measurement --- p.46 / Chapter 2.2.4. --- Statistical analysis --- p.47 / Chapter Chapter 3: --- Results / Chapter 3.1. --- The age and gender distribution in study subjects --- p.57 / Chapter 3.2. --- The HTRA1 sequencing in exudative AMD and PCV --- p.57 / Chapter 3.2.1. --- Polymorphism identification and genotypic association --- p.57 / Chapter 3.2.2. --- Haplotype structure and Haplotype-based association analysis --- p.59 / Chapter 3.2.3. --- Joint genotype analysis --- p.59 / Chapter 3.3. --- Differential association of exudative AMD and PCV with the ARMS2/HTRA1 locus --- p.60 / Chapter 3.3.1. --- Genotypic association --- p.60 / Chapter 3.3.2. --- Haplotype analysis --- p.62 / Chapter 3.3.3. --- Logistic regression --- p.63 / Chapter 3.3.4. --- Meta-analysis of ARMS2/HTRA1 association with PCV --- p.64 / Chapter 3.3.5. --- In-position OR plot --- p.64 / Chapter 3.4. --- FPR1 and CFH in exudative AMD and PCV --- p.65 / Chapter 3.4.1. --- Polymorphism identification and genotypic association --- p.65 / Chapter 3.4.2. --- Haplotype analysis of FPR1 --- p.66 / Chapter 3.4.3. --- The association of CFH rs800292 --- p.67 / Chapter 3.4.4. --- Joint effect analysis of the CFH and FPR1 genes --- p.67 / Chapter 3.4. --- Phenotype-genotype correlation in ARMS2/HTRA1 locus --- p.68 / Chapter 3.4.1. --- Distribution of age and bilaterality --- p.69 / Chapter 3.4.2. --- Greatest linear dimension of CNV lesion in exudative AMD --- p.69 / Chapter 3.4.3. --- Response to treatment in exudative AMD --- p.69 / Chapter 3.4.4. --- Recurrence in PCV --- p.70 / Chapter 3.4.5. --- Smoking status --- p.70 / Chapter Chapter 4: --- Discussion / Chapter 4.1. --- Age and gender distribution --- p.104 / Chapter 4.2. --- Genetic differentiation in ARMS2/HTRA1 locus --- p.S104 / Chapter 4.2.1. --- SNPs with common association --- p.106 / Chapter 4.2.2. --- SNPs with different association S --- p.106 / Chapter 4.2.3. --- Comparison with previous studies C --- p.107 / Chapter 4.2.4. --- Sample size S --- p.109 / Chapter 4.3. --- The FPR1 gene in exudative AMD and PCV --- p.110 / Chapter 4.4. --- Interaction between FPR1 and CFH --- p.112 / Chapter 4.5. --- Correlation between phenotypes and genotypes --- p.113 / Chapter 4.6. --- Common and rare variants for complex disease --- p.114 / Chapter 4.6.1. --- The debate of common disease common variant versus common disease rare variant --- p.115 / Chapter 4.6.2. --- Candidate gene screening versus geno-wide association study --- p.117 / Chapter 4.6.3. --- Common variants versus rare variants in 10q26 locus --- p.118 / Chapter 4.6.3.1. --- Common variants --- p.119 / Chapter 4.6.3.2. --- Rare variants --- p.120 / Chapter Chapter 5: --- Conclusions and future prospects --- p.122 / Chapter Chapter 6: --- References --- p.124