INS Early Career Research Award Recipients
Fatigue is another dopamine-dependent construct that has been shown to rely on the fronto-striatal brain regions and is a symptom that individuals with MS and TBI often experience. Given this neural common denominator between fatigue and outcome processing, I investigated whether fatigue can be reduced through engaging individuals with MS and TBI in a goal-directed behavior, showing that fatigue can be reduced through outcome presentation.
Our study challenged the retrieval deficit and the associative deficit hypotheses of memory impairments in Parkinson’s disease (PD). The former supports a memory deficit mediated by attention/executive dysfunctions, while the latter hypothesizes a genuine memory impairment in PD.
Major depressive disorder (MDD) is the most prevalent psychiatric disorder, affecting between 10 and 20 % of the world population at some point in their lives. MDD is characterized by a high risk for relapse after recovery (40% within 2 years). Therefore, understanding and changing the highly recurrent course of MDD is of high clinical and societal importance.
Much of what we know about brain-behavior relations is made possible by the study of neuropsychological cases. Given the ubiquity of functional neuroimaging studies, and the importance they have assumed in elucidating brain function, the goal of my talk is to describe how single cases continue to challenge accepted dogma, to lead to new discoveries, and to suggest hypotheses and theories that steer the field in new directions.
Katerina studied cognitive neuropsychology and theoretical psychoanalysis at University College London (UCL) before completing her PhD on the neuropsychology of confabulation at the University of Durham, UK. She is currently an Associate Professor (Reader) at the Research Department of Clinical, Educational and Health Psychology at UCL.
Memory deficits characterize Alzheimer’s disease and its clinical precursor amnestic mild cognitive impairment (aMCI). While a growing body of research furthers our understanding of the detection, characterization, and neuroanatomy of these memory deficits, the clinical translation of these findings has lagged. So, providers continue to be faced with the critical question of “What can I do about it?” Treatment is typically limited to a handful of medications that are, at best, marginally successful. This limitation has fostered a growing interest in non-pharmacologic treatment methods for minimizing learning and memory deficits, approaches that include cognitive training and cognitive rehabilitation.
Through a journey from toddlerhood to adolescence, this talk will provide a multimodal perspective of the impact of pediatric traumatic brain injury (TBI) on social functioning. The emergence of socially meaningful interactions, better perspective taking, greater social independence and more complex societal roles and responsibilities are key milestones of social development. Brain disruptions occurring at any stage along this path can disturb the delicate balance of environmental, cerebral, and cognitive processes underlying social competence, leading to inappropriate social behaviors.
As the population ages, unhealthy cognitive decline and dementia are increasingly important public health issues. Vascular risk factors, such as hypertension, diabetes mellitus, and atherosclerosis, are associated with abnormal neuroanatomic changes, cognitive impairment, and clinical dementia in older adults. A poorly understood aspect of compromised vascular health and cognitive aging is the association between systemic hemodynamics (cardiac output or the amount of blood exiting the heart to perfuse the system) and brain aging.
Dr. Brickman uses advanced neuroimaging techniques to understand cognitive aging and dementia. He is particularly interested in white matter abnormalities and the intersection between vascular disease and Alzheimer’s disease. Ongoing Research: The effect of age on neuromorphology and its cognitive consequences. His current research efforts focus primarily on “normal” cognitive and structural changes across the adult lifespan.
John Gunstad is Associate Professor in the Department of Psychology at Kent State University. He obtained a B.A. in psychology from Moorhead State University and both his M.S. and Ph.D. in clinical psychology with concentration in clinical neuropsychology from Ohio University. He completed internship and F32 postdoctoral fellowship at Brown Medical School, where he began a line of research in the neurocognitive effects of medical conditions including obesity and cardiovascular disease.