Diss. (sammanfattning) Linköping : Linköpings universitet, 2007. / Härtill 4 uppsatser.

Thesis (M.Phil.) -- Australian Catholic University, 2002. / A thesis submitted in total fulfillment of the requirements of Master of Philosophy. Bibliography: p. 102-140. Also available in an electronic format via the internet.

Thesis (Ph.D.)--Southern Illinois University at Carbondale, 2008. / Advisers: Kim Asner-Self, Tracy Stinchfield. Includes bibliographical references.

Thesis (Ph. D.)--Johns Hopkins University, 1997. / Vita. Includes bibliographical references (leaves 147-159).

Project (D. Min.)--Perkins School of Theology, Southern Methodist University, 1976. / Includes bibliographical references (leaves vii-x).

Thesis (D. Min.)--Ashland Theological Seminary, 1987. / Includes bibliographical references (leaves 170-172).

M.Sc. / Please refer to full text to view abstract

The aging process is unforgiving, targeting a decline in cellular function. Originally, the actin cytoskeleton has not been defined as a hallmark of aging biology, however, numerous studies provide evidence that actin cytoskeleton integrity is declining with age. Mammalian cells express an aged-linked decline in their actin dynamics, consequently defecting their migratory movements, immunological synapse formation, and phagocytosis. Overall, suggesting actin integrity is specifically targeted by aging. Despite the substantial evidence, the underlying mechanism remains elusive, however, current research indicates actin stability as a possible mechanistic aging target. Therefore, our research goal is to further elucidate the mechanism for actin cytoskeleton aging biology in a streamlined model organism, budding yeast, Saccharomyces cerevisiae. Here, we use aging enrichment protocols, streptavidin affinity purification, to isolate a population of older cells to examine any changes in the actin cytoskeleton with age. With an isolated aging population, we analyzed the actin cytoskeleton by testing its stability against a destabilizing drug, Lat-A, and morphology with imaging analysis. We find significant age-associated changes in the actin cytoskeleton, which we later conclude may be a consequence of the age-linked decline in the actin stability that we identified in an aging cell. Additionally, we uncovered a perplexing finding that there is an age-linked decline in actin cable bundling. How actin stability effects actin cable bundling, remains to be determined. However, our actin stability model was further supported by our research characterizing an open reading frame, YKL075C, as a novel actin cable regulatory protein whose deletion: increased actin cable stability, abundance, and mitochondrial quality to extend the replicative lifespan. Upon further insight into YKL075C underlying mechanism, we find YKL075C effects on actin stability and morphology is dependent on alterations in branched-chain amino acid (BCAA) metabolism. Overall, our research discovered a novel actin regulatory protein, Ykl075cp, whose actin function is dependent on BCAA homeostasis, and deleting specifically YKL075C reduces BCAA levels that subsequently increases actin cable stability and abundance to enhance mitochondrial quality and extends longevity.

Metamemory is “knowing about knowing” (Flavell, 1971) and is theorized as a cognitive process that monitors and controls the memory system (Flavell & Wellman, 1975; Nelson & Narens, 1990). The predominate finding in the metamemory and aging literature is that metamemory is unimpaired by aging, even when memory is impaired by aging (Eakin & Hertzog, 2006; 2012; Connor, Hertzog, & Dunlosky, 1997; Hertzog, Sinclair, & Dunlosky, 2010; Eakin, Hertzog, & Harris, 2014, but see Souchay, Moulin, Clarys, Taconnat, & Isingrini, 2007). However, a study examining metamemory for emotional words suggests older adults may show metamemory impairment when predicting memory for emotional words (Tauber & Dunlosky, 2012). This finding challenges the supposition that metamemory is unimpaired with aging. The purpose of the current study was to expand on the results from Tauber and Dunlosky (2012) to determine whether their findings were due to methodological issues rather than age-related deficits in metamemory.

No description available.