Clinical neuropsychologists assess the cognitive functioning of individuals with a wide range of psychiatric and neurological disorders. They provide feedback to patients that include both conclusions about their diagnosis and prognosis, as well as specific recommendations related to improving their everyday functioning. Despite the importance of this part of the assessment, there has been limited research on the types of recommendations that are provided to patients. The study surveyed 309 clinical neuropsychologists who work with adult patients to address this open question. The results from this research can be used to improve the lives of patients and their family members by informing best practices for what recommendations clinical neuropsychologists should give to patients with specific concerns.

The overall objective of this dissertation was to increase scientific understanding of brain reserve. Chapter 1 describes how brain reserve has come to be viewed in two distinct ways: differential expression of brain injury on the basis of individual differences in gross brain properties (neurological), or on the basis of lifespan patterns of complex mental activity (behavioural). Evidence in the Alzheimer???s disease and ageing literature has been extensive, yet with conflicting reports. In order to better evaluate this evidence, a systematic review of cohort studies is the focus of Chapter 2. Complex mental activity was found to be associated with reduced incidence of dementia and slowed rate of cognitive decline. Neurological brain reserve evidence was limited. A major task of this dissertation was to develop a more standard and complete behavioural brain reserve instrument. Chapter 3 relates the development of the Lifetime of Experiences Questionnaire (LEQ) in a group of 86 healthy elderly. The LEQ had adequate levels of internal consistency and reliability. In a validation test, higher LEQ scores were also found to predict attenuated cognitive decline over 18 months independent of covariates including premorbid IQ. Chapter 4 describes how both LEQ (as a measure of behavioural brain reserve) and intracranial volume (as a measure of neurological brain reserve) significantly predicted cognitive decline over three years in a sample of 70 aged subjects. Total LEQ was furthermore significantly correlated with hippocampal volume independent of intracranial volume, and this association mediated the relationship with cognitive decline. Behavioural brain reserve may therefore work by protecting individuals from hippocampal atrophy. The fifth chapter explores therapeutic and neurobiological aspects of behavioural brain reserve in a preliminary fashion. A randomized-control mental activity trial was run with 20 healthy elderly who received repeat magnetic resonance spectroscopy. Mental activity subjects were found to have selective and sustained upregulation of phosphocreatine metabolism in the hippocampal region, a finding of potential neuroprotective significance. Experience-dependent neuroplasticity is proposed as a unifying framework in the final chapter, allowing synthesis of the present findings and reconciliation of the neurological and behavioural approaches to brain reserve.

The objectives were to explore cognitive function in older adults with Type 2 Diabetes Mellitus (T2DM) through two studies: 1) a pilot study involving the metabolic stress of glucose ingestion and the environmental stress of a functional magnetic resonance imaging (fMRI) environment and 2) an fMRI study exploring the neural mechanisms through hippocampal and prefrontal functional imaging during memory and executive functioning tasks. In T2DM subjects, environmental stress produced greater impairment in memory performance and metabolic stress produced overestimation of memory performance, with similar executive functioning, relative to healthy subjects (pilot study). T2DM subjects also sowed reduced hippocampal and greater prefrontal activation compared to healthy subjects (fMRI study). Moreover, the metabolic stress caused greater hippocampal and prefrontal activation in healthy subjects relative to placebo (fMRI study). These results indicate plausible neural mechanisms behind T2DM- and stress-associated cognitive impairments that can be used for future improvements in cognitive retention and rehabilitation.

The objectives were to explore cognitive function in older adults with Type 2 Diabetes Mellitus (T2DM) through two studies: 1) a pilot study involving the metabolic stress of glucose ingestion and the environmental stress of a functional magnetic resonance imaging (fMRI) environment and 2) an fMRI study exploring the neural mechanisms through hippocampal and prefrontal functional imaging during memory and executive functioning tasks. In T2DM subjects, environmental stress produced greater impairment in memory performance and metabolic stress produced overestimation of memory performance, with similar executive functioning, relative to healthy subjects (pilot study). T2DM subjects also sowed reduced hippocampal and greater prefrontal activation compared to healthy subjects (fMRI study). Moreover, the metabolic stress caused greater hippocampal and prefrontal activation in healthy subjects relative to placebo (fMRI study). These results indicate plausible neural mechanisms behind T2DM- and stress-associated cognitive impairments that can be used for future improvements in cognitive retention and rehabilitation.

Thesis (Ph. D.)--University of Texas at Austin, 1999. / Vita. Includes bibliographical references (leaves 163-173). Available also in a digital version from Dissertation Abstracts.

Thesis (Ph. D.)--University of California, San Diego, 2001. / Vita. Includes bibliographical references (leaves 93-105).

Thesis (Ph. D.)--University of Texas at Austin, 2000. / Vita. Includes bibliographical references (leaves 81-88). Available also in a digital version from Dissertation Abstracts.

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