The number of people living with Alzheimer’s Disease (AD) is projected to increase dramatically over the next few decades, making the search for treatments and tools to measure the progression of AD increasingly urgent. The antisaccade task, a hands- and language-free metric, may provide a functional index of the Dorsolateral Prefrontal Cortex (DLPFC), which is damaged in the later stages of AD. Patients with AD make significantly more antisaccade errors than controls, however, performance in mild AD has remained unexplored. We hypothesized that mild patients will make more errors than controls. Thirty AD patients and 31 age-match controls completed both laptop-based and clinical versions of the antisaccade task. Two thirds of patients with AD made significantly more errors and corrected less of their errors than age-matched controls. Our findings indicate that antisaccade impairments exist in mild AD, suggesting DLPFC pathology may be present earlier than suggested by previous studies.

The number of people living with Alzheimer’s Disease (AD) is projected to increase dramatically over the next few decades, making the search for treatments and tools to measure the progression of AD increasingly urgent. The antisaccade task, a hands- and language-free metric, may provide a functional index of the Dorsolateral Prefrontal Cortex (DLPFC), which is damaged in the later stages of AD. Patients with AD make significantly more antisaccade errors than controls, however, performance in mild AD has remained unexplored. We hypothesized that mild patients will make more errors than controls. Thirty AD patients and 31 age-match controls completed both laptop-based and clinical versions of the antisaccade task. Two thirds of patients with AD made significantly more errors and corrected less of their errors than age-matched controls. Our findings indicate that antisaccade impairments exist in mild AD, suggesting DLPFC pathology may be present earlier than suggested by previous studies.

A challenge in the treatment of central nervous system (CNS) diseases is the transport of drug candidates into the brain. Inositol stereoisomers have show promise as therapeutic agents for CNS disorders. scyllo-Inositol was an effective prophylactic and therapeutic for Alzheimer’s disease (AD) in TgCRND8 mice, a model of AD. This suggests inositol stereoisomers have excellent CNS bioavailability. They enter the brain through inositol transporters, of which there are three: one hydrogen myo-inositol transporter (HMIT) and two sodium myo-inositol transporters (SMIT1, SMIT2). HYPOTHESIS: Given the high CNS bioavailability of inositol stereoisomers, it may be possible to use inositol transporters to shuttle other compounds into the CNS. OBJECTIVES: 1. To confirm the CNS bioavailability of the two main inositol stereoisomers, myo- and scyllo-inositol, in both TgCRND8 and wild-type mice. 2. To examine inositol transporter expression in the brains, as a function of time and disease pathology, in both groups. 3. To evaluate the flexibility of the inositol transporters for transporting compounds by determining the substrate structural features required for active transport. RESULTS: myo-Inositol and scyllo-inositol accumulated in the brain following oral administration. Disease pathology did not alter baseline inositol levels or uptake. Brain subregional transporter expression was unaltered as a function of age or disease pathology. In vitro cell culture experiments found HMIT inactive and therefore not a contender for drug transport. In contrast SMIT1 and SMIT2 were both active and competitive transport assays, revealed distinct criteria for active transport through each system. However, both were stringent in the substitutions to the structure of myo-inositol possible to maintain active transport. CONCLUSION: Active transport through the inositol transporters is very sensitive to changes in the structure of myo-inositol and only conservative changes are possible. Therefore, these transporters would not make effective shuttling systems for drug transport into the brain.

Alzheimer'€™s disease (AD) is the fifth leading cause of death among the elderly. This study uses National Center for Health Statistics (NCHS) Multiple Cause of Death data for the United States for the years 1998 to 2002, examining the 9.5 million death records of all decedents of age 60 and over, and determines their incidence of AD. Seven independent variables are used: age, sex, race, ethnicity, marital status, education level and whether or not they lived in a metropolitan area. This study uses logistic regression, modeling five nested models, to determine the likelihood of mortality by AD and the direction of the relationship between AD and each of the variables. A Bayesian analysis, used to determine the best fit model, found that the full model was the best fit. The major findings of the study are that the incidence of AD increases significantly with increasing age in decedents aged 60-90. However, this peaks for decedents aged 85-89. Those who survive past age 90 begin to have a lesser likelihood of mortality by AD. With the exceptions of marital status and education, the hypotheses were supported. Females are more likely to die of AD than males. NonHispanic Whites are more likely to die of AD than Hispanics and NonHispanic Blacks. There is an increased risk of dying in a nursing home if one dies of AD. Future research as outlined above is needed to learn further about this fifth leading cause of mortality of those over age 60.

Thesis (M.Med.Sc.)--University of Hong Kong, 2009. / Includes bibliographical references (p. 92-102).

Thesis (M.A.)--Central Connecticut State University, 2001. / Thesis advisor: C. Charles Mate-Kole. " ... in partial fulfillment of the requirements for the degree of Master of Arts in Psychology." Includes bibliographical references (leaves 36-44). Also available via the World Wide Web.

Thesis (M.A.)--Central Connecticut State University, 2000. / Thesis advisor: Charles Mate-Kole. " ... in partial fulfillment of the requirements for the degree of Master of Arts in [in Psychology]." Includes bibliographical references (leaves 46-60).

Thesis (M.A.)--Central Connecticut State University, 2000. / Thesis advisor: Charles Mate-Kole. " ... in partial fulfillment of the requirements for the degree of Master of Arts in Psychology." Includes bibliographical references (leaves 40-47).

Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references (leaves 159-173). Available also in a digital version from Dissertation Abstracts.

Thesis (Ph. D.)--Oregon State University, 2002. / Typescript (photocopy). Includes bibliographical references. Also available on the World Wide Web.