Thesis (M. S.)--Psychology, Georgia Institute of Technology, 2008. / Committee Chair: Paul Corballis; Committee Member: Eric Shumacher; Committee Member: Fredda Blanchard-Fields.

Thesis (Ph. D.)--University of Missouri-Columbia, 2009. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2009" Includes bibliographical references.

Thesis (M.S.)--University of Michigan, 1978.

Issued also as Thesis (Ph. D.)--Columbia University. / Bibliography: p. 29.

Thesis (Ph.D.)--Aberdeen University, 2009. / Title from web page (viewed on Dec. 2, 2009). Includes bibliographical references.

Thesis (Ph.D.)--RAND Graduate School, 2006. / Includes bibliographical references.

Normative age differences and declines in cognition may be overestimated due to influences reflecting impending mortality. The terminal decline hypothesis posits that accelerated cognitive decline for older adults is a function of proximity to death. Although previous research has demonstrated mortality-cognition associations, key questions remain unresolved. This study examined five neglected aspects of terminal decline research: (a) are mortality deficits uniform across age? (b) does impending mortality differentially influence cognitive domains? (c) does cause of death influence magnitude of mortality deficits? (d) do individuals closer to death show accelerated cognitive declines? and (e) do mortality deficits share associations with indicators of neurological disturbance such as performance inconsistency? The sample consisted of 707 adults from the Victoria Longitudinal Study (VLS) who completed between 1 to 5 waves of measurement over a 12-year period. Participants were classified as either Young-Old (59 to 79 years, M = 71.86) or Old-Old (80 to 95 years, M = 83.66). A total of 442 Survivors completed all waves and relevant measures compared with 265 Decedents who participated on at least one occasion and subsequently died. An extensive battery of tests was administered including measures of verbal speed, working memory, episodic memory, semantic memory, and crystallized verbal ability. Results were informative for each of the five research questions. First, mortality-related cognitive deficits were magnified with increasing age. Old-Old decedents exhibited steeper decline compared with similarly aged and younger survivors. Further, multilevel analyses demonstrated that Decedents declined at significantly faster rates per year increase in age. For the second research question, terminal decline was found to differentially influence select cognitive measures. Relative to Survivors, Old-Old Decedents displayed large variation across measures exhibiting poorer performance for verbal speed and episodic memory with considerably better performance for vocabulary. Results for the third research goal demonstrated that specific cause of death differentially influenced cognitive performance. Greater cross-sectional differences and declines were found for those who died of cardiovascular disease (CVD). A fourth contribution to the terminal decline literature found that the shape of cognitive decline for Decedents was accelerated in closer proximity to death. Evidence for the final research question revealed that impending death, presence of CVD, and older age were all associated with increased performance inconsistency. Considered together, these results provide both converging evidence and novel contributions to the terminal decline literature. / Graduate

No description available.

No description available.

In this study, the effect of aging on various cells of the immune system was investigated. The two experimental models used were normal young (1-2 months) and old (22-24 months) DBA/2 mice and autoimmune-susceptible young (1-2 months) and old (5-6 months) MRL-Ipr/Ipr (Ipr) mice. Autoreactive T cell clones isolated from DBA/2 mice were used to study the age-induced differential responses of syngeneic T cells and B cells. These cell interactions were found to be greatly diminished in old DBA/2 mice, and this appeared to be due to an intrinsic defect in the cells from old mice. A decreased syngeneic mixed lymphocyte reaction (SMLR) was also found to be associated with these defects in T-T and T-B interactions. The decreased SMLR was due to a reduction in the production of interleukin-1 by macrophages from old mice. In the Ipr mice, age-induced alterations in the cell surface characteristics of the abnormal T cells that accumulate in the lymph nodes were studied. The double-negative T cells from the lymph nodes of old Ipr mice were found to express a cell surface marker, J11d, that is normally present only on immature T cells in the thymus. Furthermore, the number of double-negative J11d⁺ T cells also increased in the thymus of old Ipr mice. Autoreactive T cell clones isolated from DBA/2 and /pr mice exhibited the properties of both T_H1 and T_H2 subsets as the clones secreted IL-2, IL-4 and IFN-γ, and activated both B cells and macrophages. The current study indicates that with increasing age, the autoreactive T cell-induced immunoregulation is disturbed, which may account for reduced immune responsiveness to foreign antigens and increased susceptibility to autoimmune diseases. / Ph. D.