Thesis (M.Psych.(Clinical)/Ph.D.)--University of Western Australia, 2006.

Thesis (M.A.) University of Missouri-Columbia, 2005. / 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. Title from title screen of research.pdf file viewed on (July 10, 2006) Includes bibliographical references.

Disturbances in awareness of memory deficit have been observed in Alzheimer's disease (AD), yet few studies have systematically investigated the phenomena in this population. The present study has applied the concepts and instruments used in the metamemory literature to the study of awareness of memory deficit in twenty mild AD patients, eighteen individuals with memory impairment, and eighteen normal elderly controls. Specifically, a multidimensional approach to metamemory was selected including an evaluation of perception of memory change, knowledge about memory functioning, and self-monitoring of memory performance. Consistent with previous research, AD patients reported less change in memory functioning than did their informants, suggesting that these patients have diminished awareness of the extent of the decline in their memory abilities. No differences among the three groups were observed in self-report measures addressing the use of strategies, perception of control over memory functioning, and presence of anxiety in memory-related activities. Diminished self-monitoring abilities were observed in the AD patients' tendency to make a high number of intrusion errors with few self-corrections, and to overestimate their performance on memory tests. The results also suggest that relatives' evaluation of memory functioning may be particularly useful in differentiating AD patients from older adults displaying memory impairment and from normal elderly. / Graduate

M. Tech. / Memory loss refers to the loss of ability to learn new information and the inability to retrieve information previously learnt (Karlawish & Clark, 2003). It is estimated that more than 40% of individuals over the age of 60 are affected by memory loss (Jackson, 2004). There are no recommended treatment options available for mild forms of memory loss (D‟Esposito & Weksler, 2000). The aim of the study was to determine the effects of the anthroposophical medicine, Scleron® in the treatment of memory loss associated with ageing, assessed by digit span; verbal and visual recall and recognition and a memory questionnaire. The trial was a double-blind placebo controlled study using matched pairs. Participants selected to take part in the study were between the ages of 60 and 75 and presented with subjective symptoms of memory loss. Participants were excluded from the study if they scored less than 24 out of 30 on the Mini-Mental State Exam; were previously diagnosed with memory or cognitive disorders; had a previous history of stroke, epilepsy, head injury, psychiatric disease and drug or alcohol dependence. Participants were divided into two groups in matched pairs according to age, education level, occupation and Mini-Mental State Exam scores. At the start of the study, participants completed a memory test and memory questionnaire. Participants in the experimental group received Scleron®, while participants in the placebo group received unmedicated tablets. Participants were required to take 2 tablets in the morning for a period of six weeks. The memory test and memory questionnaire was once again completed by participants at the end of the study. Thirty six participants completed the study. The results of the study were analysed and frequencies and descriptives were calculated for the sample group. The Wilcoxon test was used to compare the data within groups, while the Mann-Whitney test was used to compare the results between the two groups. iv After analysis of the results of the study, it was concluded that Scleron® did not appear to improve the symptoms of memory loss when using tests of digit span, verbal and visual recall or verbal and visual recognition. Furthermore, it did not appear to improve subjective symptoms of memory loss assessed by the use of a memory questionnaire.

As the aging population continues to grow worldwide, age-related complications are becoming more apparent within the aging population. One of the first age-related complications to become apparent is age-associated memory impairment and it can make the elderly more dependent on caregivers early on. The N-methyl-D-aspartate (NMDA) receptor is important to learning and memory and appears to be especially vulnerable to the process of aging. The density of NMDA receptors declines with age more than any other ionotropic glutamate receptor. Both the density of NMDA receptors and the mRNA and protein expression of its subunits decline with age. In particular, the GluN2B subunit of the NMDA receptor shows the greatest age-related declines in expression across multiple brain regions, including the frontal lobe (including the prefrontal and frontal cortices), caudate nucleus and hippocampus. These declines are strongly correlated to age-related declines in spatial memory. Specifically, age-related decreases in the protein expression of the GluN2B subunit within crude synaptosomes of the frontal cortex of C57BL/6 mice show a relationship to the declines in performance in a long-term spatial memory task across age groups. However, within the population of aged mice, there was a subpopulation of aged mice in which higher expression of the GluN2B subunit within the synaptic membrane of the hippocampus was associated with poorer performance in the same task. Moreover, transgenic mice designed to express higher levels of the GluN2B subunit from birth also possess superior memory, including spatial memory, across adulthood to middle-age. Taken together, these data led to the hypothesis that increasing the expression of the GluN2B subunit within the aged brain could potentially alleviate age-related declines in memory. However, increasing its expression regionally was first examined since higher expression of the GluN2B subunit within the hippocampus has been associated with poorer memory in aged animals. Since age-related decreases in the protein expression of the GluN2B subunit within the frontal cortex show a relationship to impaired memory function, the first study was designed to determine if increasing GluN2B subunit expression in the frontal lobe would improve memory in aged mice. Mice received bilateral injections of either an adenoviral vector, containing cDNA specific for the GluN2B subunit and enhanced Green Fluorescent Protein (eGFP) (GluN2B vector); an adenoviral vector containing only the cDNA for eGFP (control vector); or vehicle into their frontal lobe. Spatial memory, cognitive flexibility and associative memory were assessed using the Morris water maze. Aged mice, with increased GluN2B subunit expression in the frontal lobe, exhibited improved long-term spatial memory, comparable to young mice, in the second day of training. Moreover, a higher concentration of the specific GluN2B antagonist, Ro 25-6981, was required to impair long-term spatial memory in aged mice with enhanced GluN2B subunit expression, as compared to aged controls. The requirement for greater antagonism in aged mice to block memory performance suggests that the number of GluN2B-containing receptors in their frontal lobe was enhanced and contributed to the improved memory. This study provides suggestive evidence that therapies that enhance GluN2B subunit expression within the aged brain could have the potential to ameliorate age-related memory loss. Since higher expression of the GluN2B subunit within the hippocampus of aged mice is associated with poorer memory, the second study was designed to determine if increasing GluN2B subunit expression in the hippocampus would improve or further impair memory in aged mice. This would help to determine if a therapy aimed at enhancing the GluN2B subunit expression or function of GluN2B-containing receptors throughout the aged brain could help ameliorate age-associated memory loss. Mice were injected bilaterally with either the GluN2B vector, a control vector or vehicle into the hippocampus. Spatial memory, cognitive flexibility and associative memory were assessed using the Morris water maze. Aged mice, with increased GluN2B subunit expression in the hippocampus, exhibited improved long-term spatial memory, comparable to young mice, early in training. However, there was a trend for impaired memory later in the long-term spatial memory trials. Still, these data suggest that enhancing GluN2B subunit expression in the aged hippocampus could be more beneficial to memory than harmful. In addition, the results of this study suggest that enhancing GluN2B subunit expression in different brain regions may improve memory at different phases of learning. Therefore, therapies that enhance GluN2B subunit expression throughout the aged brain could help ameliorate age-related memory loss. The first two studies demonstrated that enhancing the expression of the GluN2B subunit within either the frontal lobe or hippocampus of the aged brain has the potential to reduce age-related memory declines. However, the increase was not global nor specific to the synapse. Therefore, a third study was developed with the intent of garnering a more global increase in GluN2B subunit expression that was localized to the synapse. Cyclin dependent kinase 5 (Cdk5) enhances endocytosis of the GluN2B subunit-containing NMDA receptors from the synapse. Previous research has shown that inhibiting Cdk5 increases the number of GluN2B subunits at the synapse and within the whole cell and improves memory in young mice. This study was designed to determine if using antisense phosphorodiamidate morpholino oligomers (Morpholinos) to decrease the expression of Cdk5 protein within the brain would improve memory in aged mice. Morpholinos were conjugated to a cell penetrating peptide, which enhances cellular uptake, and delivered bilaterally to the lateral ventricles of both young and aged mice via acute stereotaxic injection. Treatments consisted of equivalent volumes and concentrations of either vehicle, control Morpholino or a Morpholino targeting the mRNA of Cdk5 (Cdk5 Morpholino). Memory was evaluated in the Morris water maze and using a novel object recognition task. Aged mice treated with the Cdk5 Morpholino exhibited improved early acquisition and spatial bias in the long-term spatial memory trials, as well as improved performance overall, compared to control Morpholino-treated aged animals. However, aged mice treated with the Cdk5 Morpholino performed similarly to vehicle-treated aged animals. The presence of the peptide-conjugated Morpholinos within the brain may have worsened performance in the Morris water maze task since control Morpholino-treated animals performed significantly worse than vehicle-treated animals. In concurrence, there was significantly greater gliosis in peptide-conjugated Morpholino-treated animals over vehicle-treated brains, suggesting it was neurotoxic. In contrast, young mice treated with the Cdk5 Morpholino showed impaired early acquisition and spatial bias but a trend for improved later learning in the long-term spatial memory task compared to control Morpholino-treated animals. Treatment with the Cdk5 Morpholino had no significant effect on cognitive flexibility, associative memory or novel object recognition for young or aged animals. Immunohistochemistry revealed increased GluN2B subunit expression within cells with characteristics of neurons and astroglia in regions of the frontal lobe, caudate nucleus and hippocampus of aged mice who received the Cdk5 Morpholino compared to control treatments. However, the increased GluN2B subunit expression appeared to be greater within the hippocampus. These results suggest that inhibiting the translation of Cdk5 using Morpholinos increased GluN2B subunit expression in both young and aged mice and may have contributed to the improved long-term spatial memory observed in aged mice, despite the Morpholino being administered at a presumably toxic concentration. An additional group of mice was used to determine a non-neurotoxic dosage of the peptide conjugated Morpholino. However, future studies are needed to determine the efficacy of the Cdk5 Morpholino at this dosage. Taken together, the studies presented here suggest that increasing expression of the GluN2B subunit within the aged brain does improve age-associated memory declines. In addition, cell penetrating peptide- conjugated Morpholinos show promise as tools for genetic manipulation within the brain and Cdk5 could prove to be a novel target for enhancing GluN2B subunit expression within the aged brain. Though future studies are needed, the studies presented here do suggest that therapies that enhance GluN2B subunit expression within the aged brain have the potential to help ameliorate memory loss. However, since enhanced GluN2B subunit expression itself can increase the potential for excitotoxicity, an optimal dose of such a therapeutic would need to be determined. / Graduation date: 2013

M.Tech (Homoeopathy) / The aim of this study is to determine the influence of homoeopathically prepared Ginkgo Biloba 6X potency compared with that of phytotherapeutically prepared Ginkgo Biloba Extract; on the results of psychometric tests used to ascertain short-term memory loss in the geriatric subject. 21 elderly volunteers received; Ginkgo Biloba Extract (500mg), a homoeopathic 6X potency of Ginkgo Biloba and a placebo according to a double blind design. One hour after administration of the treatment, volunteers were subjected to psychometric testing namely the Reading Comprehension Test, which serves to assess the status of the short-term memory. No statistically significant changes from the placebo were observed in either of the groups. Adjusted scores for education and Mini Mental Status Exam scores however revealed a positive trend in favour of the homoeopathic 6X potency of Ginkgo Biloba Further evaluation with a larger study sample could provide more conclusive evidence as to its efficacy

Two skills necessary for the execution of proficient calculation, retrieving arithmetic facts from memory and accessing number magnitude information, were studied in a group of patients diagnosed with Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy controls to try to elucidate the locus of impairment in AD-related calculation deficits. This was achieved through the use of an arithmetic production task and a number-matching task as measures of explicit and implicit retrieval of arithmetic facts, and a numerical Stroop task that assesses automatic access to number magnitude representation. AD patients, but not MCI patients, showed high response latencies and a high number of errors when performing multiplications in the production task, and reduced automatic retrieval of arithmetic task in the number-matching task. All participants showed the classic problem-size effect often reported in the mathematical cognition literature. Performance on the numerical Stroop task suggests that access to number magnitude information is relatively resistant to cognitive impairment. ... Results for the AD group are consistent with a pattern of preserved and impaired cognitive processes that might mediate the reported calculation deficits in AD. / by Marâia Beatriz Jurado Noboa. / Thesis (Ph.D.)--Florida Atlantic University, 2013. / Includes bibliography. / Mode of access: World Wide Web. / System requirements: Adobe Reader.

[Truncated abstract] The aim of the present series of studies was to identify barriers to working memory for multifeature visuospatial stimuli in normal aging. Memory for multifeature stimuli requires retention of multiple visuospatial features, as well as the relationships between features within stimuli, known as memory binding. In Experiment 1, younger people (17-25 years) and older people (66-95 years) completed a modification of Wheeler and Treisman’s (2002) visual change detection task, to determine the effects of normal aging on memory binding, and memory for multiple features ... Results indicated that older people did not have a memory binding decrement compared to younger people. Further, younger people performed more accurately when cued to attend to a specific feature, while older people’s performance did not improve with cueing ... Experiment 2 employed the binding condition and the ‘either’ condition, with stimuli presented either sequentially or simultaneously. Results were consistent with Experiment 1, with no age-related binding decrement, regardless of the method of stimulus presentation. In Experiment 1, older people demonstrated a shape memory decrement compared to younger people. Experiments 3A and 3B were performed to determine whether this result did represent a memory decrement per se, or whether it was a consequence of a shape perception decrement ... Compared to younger people, older people demonstrated a similar performance decrement across shape perception and memory tasks, indicating that their performance was mediated by an underlying perceptual decrement. Experiment 4 was conducted to determine if older people had difficulty selectively attending to a feature across multifeature stimuli, as suggested by their failure to benefit from cueing in Experiment 1 ... Older people had a greater performance decrement when the irrelevant feature was incompatible with the correct response, compared to younger people, consistent with a selective attention decrement. Experiment 5B adapted the design of Experiment 4 to both a perception task and a working memory task, while Experiment 5A identified appropriate stimulus features to use in Experiment 5B ... Overall, older people do not have particular difficulty remembering multiple visuospatial features, or binding these features within working memory. Rather, older people’s performance was marked by difficulty selectively attending to a specified feature across multifeature stimuli.

No description available.

Although not all persons with mild cognitive impairment (MCI) go on to develop Alzheimer's disease (AD), MCI is recognized as an early stage of AD. The effects of AD are devastating to all concerned. Research has identified that recognition of AD in its earliest stages and institution of known treatment modalities can forestall the ultimate outcome. Identification of the first subtle signs of MCI can assist in the recognition of this prodromal phase, and allow for institution of therapy while still in the initial stages. Unfortunately, the development of MCI is insidious in nature, thus making it difficult to detect. The purpose of this study was to identify areas of functional decline that occur in MCI in an effort to improve its early identification. A mixed-methods design that combined qualitative and quantitative methods was used. Fifty-three participants with memory complaints were interviewed using a semi structured interview technique with open-ended questions, the Montreal Cognitive Assessment (MoCA), the Geriatric Depression Scale (GDS) and a list of eighty-five items previously identified as indicative of functional decline. Twenty-nine persons were divided into two groups: 1) those identified as probable MCI (consensus diagnosis) (n=15) and possible MCI (based on screening examination) (n=14) and 2) those identified as Normal (no cognitive impairment) (n=10), and their subjective functional deficits compared. The findings suggest that there were certain areas of functional decline more commonly experienced by persons in the MCI group than by unimpaired. These include difficulty recalling details of information and forgetting conversations. There were also other changes identified, such as adaptations on the part of persons with MCI (an increased dependence on memory aids, for example, lists and calendars) and a dec rease in social activities leading to an increase in social isolation. Additionally identified were functional activities that appear to remain intact in persons with early MCI. This study highlights the subtlety with which MCI assaults the functional abilities of individuals, thus making its early identification problematic. The results of this study will contribute by providing information that will help professionals who are assessing persons experiencing memory issues for the possible presence of MCI. Additionally, it is hoped that these findings will assist in the development of a measurement tool designed to assess for possible MCI. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2015. / FAU Electronic Theses and Dissertations Collection