Thesis (Ph.D.)--Drexel University, 2010. / Includes abstract and vita. Includes bibliographical references (leaves 105-113).

Thesis (Ph.D.)--Duquesne University, 2005. / Title from document title page. Abstract included in electronic submission form. Includes bibliographical references (p. 175-182) and index.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 2005. / Includes bibliographical references (leaves 113-124). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 2005. / Includes bibliographical references (leaves 113-124).

Thesis (Ph. D.)--Georgia State University, 2006. / Title from title screen. Cecelia G. Grindel, committee chair; Laura P. Kimble, Frank Whittington, Carolyn Kee, committee members. Electronic text (220 p. : ill.). Description based on contents viewed May 2, 2007. Includes bibliographical references (p. 114-136).

Thesis (M.M.) Florida State University, 2006. / Advisor: Alice-Ann Darrow, Florida State University, College of Music. Title and description from dissertation home page (viewed 6-22-07). Document formatted into pages; contains 65 pages. Includes biographical sketch. Includes bibliographical references.

BACKGROUND: Dementia is the leading cause of dependence and disability in the elderly population worldwide. Effectively addressing the growing burden of dementia requires an understanding of the predictors of dementia in order to develop preventive strategies. Therefore, identifying potential associations between certain demographic and lifestyle characteristics and dementia may illuminate strategies for reducing the risk of dementia. This research analysis aims to highlight associations between demographic and lifestyle factors in midlife and dementia in later adulthood. METHODS: This is a secondary analysis of data that was collected as part of a longitudinal, prospective cohort study. Data from the Framingham offspring cohort was analyzed using the Cox proportional hazards regression model to examine the associations between the demographic and lifestyle characteristics and the risk of developing dementia. The multivariate analysis controlled for medical history factors that may also impact dementia risk. RESULTS: There were 2462 dementia-free participants (aged ≥ 40 and ≤ 65 years) at baseline at the time of the 2nd exam cycle, during which all demographic, lifestyle, and medical history factors were collected. During the follow-up period, 286 dementia events were observed (11% of participants). In univariate models, advanced age was significantly associated with an increased risk of dementia, while education level, alcohol use (vs. no use), and wine consumption demonstrated statistically significant protective effects against the development of dementia. After controlling for medical history in the multivariate model, older age remained a significant risk factor for dementia. CONCLUSION: This study supports established research regarding the relationship between advancing age and increased risk of dementia, and this significant association remained constant when controlling for factors such as gender and medical history. Further, the associations observed between alcohol consumption, and specifically wine, and dementia risk support continued research on alcohol use and its relationship with dementia; while these protective effects did not remain statistically significant in the multivariate model, other studies have observed significant associations between alcohol and dementia risk in adjusted analyses. Additional research would be helpful to further examine if there are any potential protective effects of alcohol, and determine whether consumption is a worthwhile preventative strategy. Overall, identifying potential risk factors for dementia is an important focus of study, due to the aging worldwide population, and the corresponding increasing significance of this disease. This analysis adds to the literature regarding the associations between certain demographic and lifestyle characteristics and the risk of dementia.

Decreased mitochondrial function is associated with aging and is an early step in Alzheimer's disease (AD). Autophagy also declines with age and is required for degradation of dysfunctional mitochondria but it is not known whether autophagosomal formation is overactive and/or degradation of autophagosomes is inhibited in AD. Although two-thirds of the 5 million Americans diagnosed with AD are women, without a clear mechanism. Since the role of gender and autophagy in AD is unclear, we wanted to know whether: A) decreased mitochondrial biogenesis precedes brain plaque formation, neuronal death and memory deficits B) autophagosomal formation is overactive and/or degradation of autophagosomes is inhibited in AD and C) deficits in mitochondrial biogenesis and autophagy occur earlier in life in the hippocampus/cortex of female AD-Tg, than male AD-Tg mice. To answer these questions, mitochondrial DNA (mtDNA), TFAM (transcription factor A mitochondrial) and two stages in autophagy, autophagosomal formation and degradation were measured in the hippocampus/cortex of non-transgenic (non-Tg) and the APP(Swe, DI)/NOS2-/- AD mouse model (AD-Tg) from 2 mo. through 12 mo. of age, when memory deficits develop. Male and female mice were evaluated for gender differences. By measuring mitochondrial gene copy number relative to nuclear gene copy number by qPCR, we found female specific decreases in mtDNA and TFAM protein levels in AD-Tg hippocampus/cortex, before 12 mo., when memory deficits develop. The male AD-Tg mice did not show any decline in the levels of mtDNA or TFAM protein through 12 mo. of age, indicating a decline in mitochondrial biogenesis earlier in life in female AD-Tg mice, than males. To determine whether autophagosomal formation is overactive and/or autophagosomal degradation is inhibited in AD, non-Tg and AD-Tg mouse neurons from 2-12 mo. of age were cultured and transfected with an adenovirus expressing the dual fusion protein, mCherry-GFP-LC3B. This system enables the distinction of early (autophagosomal formation) from late (autophagosomal degradation) stages of autophagy. Autophagosomal formation increased in female AD-Tg mice, while male AD-Tg neurons have decreased formation of autophagosomes, compared to non-Tg. Neurons from AD-Tg mice show deficits in degradation of autophagosomes by 2 mo. Our results show increased autophagosomal formation in female neurons with age and in our AD-like model without corresponding increases in degradation of autophagosomes. All together, our data indicates that the presence of familial APP mutations and knockout of NOS2 increases deficits in both mitochondrial biogenesis and autophagy in female mice, compared to males. These deficits occur before amyloid plaque formation and memory deficits, suggesting that mitochondrial and autophagic deficits may play a role in the higher incidence of AD in females.

The indirect influence of prior experience on a subsequent task is termed Implicit memory (IM). This study examined the status of pictorial and verbal IM in four groups of 20 subjects each: normal young (M age = 27.2), young-old (M age = 66.7), old-old (M age = 76.6), and Alzheimer's disease (AD) patients (M age = 75.4, M Mini-Mental State Examination score = 17.3). Study conditions involved reading words, naming pictures, and generating best-fit endings for high-cloze sentence frames (e.g., Ron swept the floor with a ____ .). Implicit memory was subsequently assessed by word-stem completion (WSC), in which subjects were instructed to complete three-letter stems with the first word that came to mind (e.g., bro____), and picture-fragment identification (PFI), in which subjects attempted to identify perceptually degraded pictures. Among the control groups, WSC priming was greatest following word study, and PFI priming was greatest following picture study, thereby establishing that crossover priming effects recently found among young subjects are fully retained in healthy aging, In contrast to previous studies suggesting that WSC priming may be preserved for deeply encoded material in AD patients, the present results showed that WSC priming was impaired in the AD group regardless of study condition, Nevertheless, AD patients demonstrated normal perceptual priming on the PFI task following picture study, These findings support a dissociation between perceptual and conceptual priming in AD. Explicit yes/no recognition testing revealed standard picture superiority and generation effects among controls. AD patients, in contrast, were impaired on all recognition items. Results are discussed in terms of transfer-appropriate processing theory, which states that level of retention Is a function of the degree to which processes invoked at study are recapitulated at test. Essentially, the similarity between word reading and WSC and between picture naming and PFI is a crucial determinant of priming effects In healthy young and elderly subjects. AD patients' WSC impairment may be due to a lexical-semantic processing deficit, whereas their preserved PFI priming may be supported by intact perceptual processes. Similarly, their uniformly depressed recognition memory may be explained by impaired conceptual processing. / Graduate

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