Browsing by Author "Longman, Richard Stewart"

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    Diffusion Tensor Imaging and Cognition of Transient Ischemic Attack Patients and Healthy Controls
    (2018-05-11) Tariq, Sana; Barber, Philip A.; Longman, Richard Stewart; Smith, Eric Edward
    Currently, there is no cure for dementia and prevention trials need to be redesigned with a focus on high-risk population and standardized biomarkers, which include clinical, demographic, imaging and neuropsychological considerations. Transient Ischemic Attack (TIA) patients are at an increased risk of dementia due to the presence of vascular risk factors and underlying vascular/neurodegenerative pathology. We hypothesized that at baseline TIA patients will exhibit abnormal microstructural white matter (WM) changes as measured by diffusion tensor imaging (DTI) parameters, and that these parameters will predict worse cognitive outcomes. Our results suggest that TIA patients showed higher axial diffusivity (AxD), mean diffusivity (MD) and radial diffusivity (RD) parameters in the fornix, a tract crucial for memory, and lower fractional anisotropy (FA) overall when compared to healthy controls. TIA patients also performed poorer on tests of executive function, episodic and working memory, and processing speed. DTI parameters of FA and MD predicted performance in tests of executive function and memory but not processing speed. Considering these results, TIA patients are a high-risk population for cognitive change.
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    Effect of age, sex and aerobic exercise on cerebrovascular regulation in older adults: Results from the Brain in Motion Study
    (2019-09-17) Wyer, Leanna; Poulin, Marc J.; Phillips, Aaron Alexander; McDonough, Meghan H.; Longman, Richard Stewart
    Background: By 2024, 20% of Canada’s population will be 65 and older. Aging is associated with progressive declines in cerebrovascular and cognitive function and an increased prevalence of age-related diseases such as Alzheimer’s Disease (AD). Physical activity has been associated with improvements in cerebrovascular function and cognitive performance, and may help to prevent and/or delay AD. However, the underlying time-course by which enhanced physical activity may be protective for brain health and differences between men and women is poorly understood. Objective: To determine the influence of age and sex on the cerebrovascular responses to submaximal exercise and euoxic hypercapnia in older adults. Furthermore, this study assessed the effects of a 6-month aerobic exercise intervention on cerebrovascular measures and evaluated outcomes after three and six months of exercise. Design: 202 participants aged 66.5 ± 6.5 years (mean ± SD, 101 females) completed the aerobic exercise intervention. Measurements took place pre-, mid- and post-intervention including demographic information, maximal aerobic capacity (VO2max) and cerebrovascular function. Linear mixed models adjusted for covariates were used to measure the physiological responses to submaximal exercise and euoxic hypercapnia pre-intervention and the changes in middle cerebral artery peak blood flow velocity (VP), mean arterial pressure (MAP) and cerebrovascular resistance (CVRi) and conductance (CVCi) indices after three and six months of aerobic exercise. Results: Pre-intervention, both age and sex were significant predictors of VP (p=0.002; p<0.010), CVRi (p<0.001; p=0.029), and CVCi (p<0.001; p=0.004) during exercise. Compared to rest, acute exercise led to increases in VP, CVRi and MAP and decreases in CVCi (p<0.001). Three months of aerobic exercise led to increases in VP (p=0.005) and CVCi (p=0.021) and decreases in CVRi (p=0.002) in women only, with no further changes observed after an additional three months of exercise. Conclusion: Male sex and increasing age were associated with lower VP, CVCi and higher CVRi. Three months of aerobic exercise led to improvements in cerebrovascular measures in women that were maintained in the latter three months of the intervention in healthy, older adults. Such results have important implications for the role of physical activity in improving health outcomes and the differences observed with aging and sex.
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    The Etiology of Long-Term Stable Mild Cognitive Impairment
    (2020-06-26) Sharma, Manu Jairam; Callahan, Brandy L.; Konnert, Candace A.; Longman, Richard Stewart
    Mild cognitive impairment (MCI) is referred to as the prodromal phase of a progressive disease (i.e., neurodegeneration) that results in dementia, however a substantial portion (ranging from 5-30%) remain cognitively stable over the long term (sMCI). The etiology of sMCI is unclear but may be due to cerebrovascular disease (CVD) and/or neuropsychiatric symptoms. The purpose of this study is to empirically determine whether CVD and neuropsychiatric symptoms are significant contributors to cognitive impairment, in the absence of neurodegenerative pathology, in individuals with sMCI. A retrospective analysis was performed on neurodegenerative and CVD data acquired at autopsy and in vivo measures of neuropsychiatric symptoms from the National Alzheimer’s Coordinating Center data repository. Individuals with sMCI (n = 28) were compared to those with MCI who declined over a 5 to 9-year period (dMCI; n = 139) on measures of neurodegenerative pathology, CVD, and neuropsychiatric symptoms. Neurodegenerative pathology (i.e., amyloid plaques, neurofibrillary tangles, and cerebral amyloid angiopathy) was significantly higher in the dMCI group compared to the sMCI group. Microinfarcts were the only CVD pathology that was associated with group membership; these were more frequent in the sMCI group compared to the dMCI group. Neuropsychiatric symptoms, measured using the Geriatric Depression Scale and the Neuropsychiatric Inventory Questionnaire, showed no difference between groups. In conclusion, the findings suggest that the etiology of sMCI is not primarily due to neurodegenerative disease, and CVD (excluding microinfarcts) and neuropsychiatric symptoms contribute to cognitive impairment similarly in both the sMCI and dMCI groups. Microinfarcts appear to contribute significantly to the cognitive impairment in sMCI and may be occurring in isolation.
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    On the Malleability of Human Cognition: Working Memory Training and Transfer
    (2017) Clark, Cameron; Goghari, Vina; Campbell, Tavis; Longman, Richard Stewart; Goodyear, Bradley; Ramasubbu, Rajamannar; Yang, Lixia
    Training working memory (WM) to increase WM capacity and fluid intelligence (Gf) has received much experimental attention in recent years, though its efficacy remains highly controversial. The current study investigated the effect of a randomized six-week online WM intervention on cognitive abilities and patterns of neural activation in a community-recruited sample of healthy young adults, in relation to both a processing speed training active control condition, as well as a no-contact control condition. Results of this randomized trial are discussed in three parts: Chapter 2 examines group-level fMRI activation patterns for tasks of WM and Gf before the training intervention. Consistent with previous research, results indicate large areas of fronto-parietal activation in response to increasing task demands for our WM task, which largely subsume more circumscribed regions of activation for our Gf task. These results are discussed in terms of a task-general central network which may underlie performance of WM, Gf, and perhaps even goal-directed behaviour more generally. Chapter 3 investigates potential differences in a wide range of cognitive test scores before and after WM training, processing speed training, or no-contact. Results revealed support for the null hypothesis across all cognitive tests administered. Because these results are consistent with experimental trials of equal or greater methodological rigor, we suggest that future research re-focus on promising interventions known to increase memory performance in healthy young adults; and/or examine alternative populations in which WM training may be efficacious. Chapter 4 examines potential differences in pre- and post-training patterns of neural activation for WM and Gf tasks in our WM training, and processing speed training groups. Results indicated significant post-training reductions in activation for the WM trained group in relation to the processing speed group for the WM task, but not the Gf task. These results suggest that WM training does not affect patterns of neural activation for Gf tasks. We suggest that future research investigate neural correlates of WM training in populations for which WM itself is impaired; and/or WM training interventions in populations that have returned more promising results compared to those with healthy young adults.
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    Reward-Related Decision-Making Among Individuals with Current and Past Disordered Gambling: Implications for its Role in the Maintenance of Problem Gambling Behaviour
    (2018-07-17) Schluter, Magdalen Grace; Hodgins, David; McGrath, Daniel S.; Callahan, Brandy L.; Longman, Richard Stewart
    Aberrant reward-related decision making is robustly associated with Gambling Disorder (GD). However, its precise role in the etiology of GD is not yet understood. This study investigated the possible role of two aspects of reward-related decision making, delay discounting (DD) and probabilistic discounting (DD), in the maintenance of GD. Additionally, it investigated the potential moderating role of substance misuse on the association between DD and GD. 434 participants with symptoms of current or past GD and symptoms of current or past substance use disorder (SUD), as well as healthy controls completed online self-report questionnaires of gambling participation, GD and SUD symptomology, and a randomly adjusting DD and PD task. Overall, the findings suggest that PD may be involved in the maintenance of GD, while DD may have greater involvement in the etiology of GD.
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    The effects of sleep deprivation and poor sleep quality on Emotional Empathy: the behavioral and neural mechanisms in healthy controls
    (2017) Guadagni, Veronica; Iaria, Giuseppe; Protzner, Andrea; Antle, Michael Christopher; Longman, Richard Stewart; Carrier, Julie
    This dissertation describes a series of experiments exploring the intricate relationship between sleep and Emotional Empathy, i.e., the ability to understand someone else’s emotions through vicarious sharing. First, I used a sleep deprivation protocol, in which sleep quality was experimentally manipulated, to test the hypothesis that sleep deprivation negatively affects the Emotional Empathy of healthy individuals (Chapter 3). The findings of this study revealed a blunting of Emotional Empathy responses across all valences for participants in the sleep deprivation group compared to participants in the control groups. I then tested the hypothesis that sleep quality accounts for variability in individuals’ empathic responses by looking at effects of natural occurring changes in sleep quality on Emotional Empathy (Chapter 4). In this study, I collected subjective (questionnaires) and objective (actigraphy) measures of sleep and used a sophisticated statistical analysis to reduce the number of collected sleep variables and generate independent factors that were then entered into a series of stepwise regressions. The results of this study showed that the subjective sleep quality factor best explained participants’ Emotional Empathy responses to negative images compared to neutral, while the total sleep duration factor best explained overall Empathy scores. Finally, to test the hypothesis of a modulatory role of sleep quality on the neural activity of areas identified as components of the Emotional Empathy network, I conducted a Region of Interest (ROI) analysis, and measured Blood Oxygen Level Dependent (BOLD) signal change while participants performed an Emotional Empathy task. In addition, I tested the effects of sleep quality on the task based functional connectivity between the selected ROIs. The data revealed decreased BOLD signal change in a selective region within the left anterior insula for individuals with poor subjective sleep quality together with increased functional connectivity between subcomponents of the anterior insula, indicating lower functional specialization. Overall, these studies suggest a detrimental effect of poor sleep quality on Emotional Empathy and its underlying neural mechanisms. These findings could benefit individuals affected by sleep disorders but also bring insight on the importance of considering sleep loss in daily life as a detrimental factor when planning work schedules.
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    Whole-Brain Atrophy Rates, Regional Cerebral Blood Flow, and Cognitive Profiles of Transient Ischemic Attack Patients and Controls
    (2019-06-18) Reid, Meaghan; Barber, Philip A.; Sajobi, Tolulope T.; Coutts, Shelagh B.; Longman, Richard Stewart
    Dementia is one of the most common causes of disability amongst the old and the prevalence is expected to double within the next twenty years. Recent prevention trials have failed to find a cure, likely due to inappropriate trial selection and a lack of reliable outcome measurements. Standardized clinical, demographic, imaging and neuropsychological biomarkers will improve selection criteria and therapeutic interventions. Transient ischemic attack (TIA) patients are at an increased risk of late-life cognitive decline due to their common vascular risk factors with dementia and underlying cerebrovascular pathology. We hypothesized that TIA patients would have increased longitudinal rates of cerebral atrophy as measured by T1 magnetic resonance (MR) imaging compared to non-TIA controls over 1 year and that increased cerebral atrophy rates would be associated with poorer cognitive outcomes. Secondly, we hypothesized that at baseline TIA patients would have lower regional cerebral blood flow (CBF) as measured by arterial spin labelled (ASL) MR imaging compared to non-TIA controls, and that CBF would be associated with cognition. Our results suggest that TIA patients show almost double the cerebral atrophy rates of non-TIA controls over 1-year, and in the absence of demonstrated change in cognition, supports that these subjects with TIA are in a preclinical stage of cognitive decline. Our results also show that TIA patients have reduced CBF in the left entorhinal cortex, the posterior cingulate bilaterally and the right precuneus which was associated with poorer memory outcomes. These predictors of early neurodegeneration and vascular changes show that TIA patients are a high-risk population for dementia and could improve inclusion criteria for clinical trials to prevent dementia in the future.