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Jason M. Watson, Ph.D. Departments of Psychology and Neurology Center on Aging

Individual Differences in Controlled Cognition. Jason M. Watson, Ph.D. Departments of Psychology and Neurology Center on Aging Center for Alzheimer’s Care, Imaging, & Research The Brain Institute University of Utah Email: jason.watson@psych.utah.edu Phone: 801-581-5040.

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Jason M. Watson, Ph.D. Departments of Psychology and Neurology Center on Aging

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  1. Individual Differences in Controlled Cognition Jason M. Watson, Ph.D. Departments of Psychology and Neurology Center on Aging Center for Alzheimer’s Care, Imaging, & Research The Brain Institute University of Utah Email: jason.watson@psych.utah.edu Phone: 801-581-5040

  2. Academic Interests As a Cognitive Scientist,my overarching research goal is to use scientific methods to investigate brain-behavior relations. Given the inter-disciplinary nature of Cognitive Science, I employ a combination of methods from Cognitive Psychology, Neuropsychology, and Cognitive Neuroscience to investigate controlled cognition including: • measuring reaction times & accuracy • measuring memory performance • cross-population studies • functional neuroimaging

  3. What Is Cognitive Control? • One of the primary functions of working memory is cognitive control. • Cognitive control refers to how working memory is used to maintain task goals in the presence of interfering or distracting information. • Individual differences in working memory capacity will influence behavioral performance in cognitively challenging tasks where interference must be minimized. • The neural substrates of controlled cognition are in prefrontal cortex. Kane & Engle (2002)

  4. Cognitive Control and Distraction Kane & Engle (2002) Watson, Bunting, Poole, & Conway (2005)

  5. Controlled Cognition and the Frontal Lobe

  6. Inducing false memoriesvia semantic associates bed rest awake tired dream night comfort drowsy yawn slumber snore pajamas sleep Deese (1959)Roediger & McDermott (1995) Roediger, Balota, & Watson (2001)

  7. Two Factor Theory • Automatic Spreading • of Activation • Controlled Monitoring Roediger, Watson, McDermott, & Gallo (2001)

  8. Additional Evidence for Two-Factor Theory Of Associative Memory Illusions Presentation Duration Aging & Dementia Probability of Recall Functional Neuroimaging McDermott & Watson (2001) Watson, Balota, & Sergent-Marshall (2001) McDermott, Petersen, Watson, & Ojemann (2003)

  9. Individual Differences in Working Memory Capacity and Associative False Memories Watson, Bunting, Poole, and Conway (2005; Experiment 2, JEP:LMC) • Tested 100 young adults with varying levels of WMC • 25 subjects/cell in a between-subjects factorial crossing of WMC (high vs. low span) with a warning manipulation (present vs. absent) using the Deese-Roediger-McDermott or DRM false memory paradigm • All participants received 5 study/test trials (i.e., practice). • Prediction: All subjects were expected to benefit from practice but only high spans were expected to benefit from forewarning. Watson, Bunting, Poole, & Conway (2005)

  10. Individual Differences in Working Memory Capacity and Associative False Memories Conclusion: Low spans had difficulty actively maintain task goal (warnings) intended to reduce susceptibility to false memories. Repeated study-test trials (practice) afforded greater environmental support to suppress false memories. Watson, Bunting, Poole, & Conway (2005)

  11. A Primer on Working Memory Capacity Tasks Conway, Kane, Bunting, Hambrick, Wilhelm, & Engle (2005)

  12. Summary & Conclusions – Part I • Activation-monitoring theories can explain DRM false memories. • Individual differences in working memory capacity may reflect underlying variability in frontally-mediated cognitive control. • Low spans may be less able to control false recall in the DRM paradigm via forewarning manipulations (Watson et al., 2005). • However, low spans can use forewarnings to reduce memory illusions – so long as you are using episodic recognition tests. • Recognition memory tests may offer participants greater environmental support to compensate for cognitive control deficits.

  13. Localizing Impairment in Executive Function in Early Alzheimer’s Disease with Neuroimaging • Memory loss is the cardinal, clinical symptom of Alzheimer’s disease. • There is increasing evidence that executive function or working memory is also compromised early in the disease with a prominent role for prefrontal cortex in goal-directed, controlled cognition. • Change in executive function in Alzheimer’s disease (AD) can be documented with carefully designed experimental procedures. • GOAL: Use advances in neuroimaging technology in combination with neuropsychological testing to determine the neural mechanisms of cognitive change in early AD.

  14. Localizing Impairment in Executive Function in Early Alzheimer’s Disease with Neuroimaging • HYPOTHESIS: Functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), and neuropsychological testing will localize the breakdown in executive function in early AD to frontal cortex. • PREDICTIONS: (1) fMRI will reveal decreased neural activity in prefrontal cortex due to increased plaque burden in early AD. (2) DTI will reveal impaired white matter functional connectivity with prefrontal cortex in early AD. (3) Neuropsychological testing will reveal deficits in executive function mediated by prefrontal cortex in early AD.

  15. Cognitive Control and Goal Maintenance in the Simon Task Castel, Balota, et al. (2007)

  16. Why is the Simon Task Optimal? • Healthy older adults and AD patients differ behaviorally on this task.

  17. Simon Says AD Patients Lose Cognitive Set with Deficits in Executive Function Castel, Balota, et al. (2007)

  18. Why is the Simon Task Optimal? • Healthy older adults and AD patients differ behaviorally on this task. • The Simon task is a relatively process-pure measure of executive function with minimal memory demands. • The Simon task activates the executive function network including prefrontal cortex and anterior cingulate (Peterson et al., 2002). • The Simon task can be administered quickly (about 45 min.) and on two occasions to assess its reliability and validity.

  19. High Span High Congruency

  20. Summary & Conclusions – Part II • The Simon task is optimal for investigating individual differences in cognitive control and goal maintenance. • AD deficits in Simon task may be due to breakdowns in prefrontal cortex and erosion of executive functions/cognitive control. • Investigations of cognitive control and reaction time distributions in young adults may offer predictions for age- or dementia-related changes in executive function. • High span young adults may attempt to automate control functions, resulting in decreased tails of RT distributions and increased errors. • Reactive vs. proactive control AND relative degradation with age/AD.

  21. Status Report and Future Directions • Enrolled 10 healthy older adults who have already completed neuropsychological testing. Scanning to commence in March. • Actively recruiting AD patients who have already completed neuropsychological testing as part of their routine clinical care. • Data analysis, data analysis, data analysis (spring/summer 2008). • Grant writing and submission (fall 2008) using pilot data obtained to justify application of protocol to patient populations who may be at risk for developing AD (e.g., Mild Cognitive Impairment). • Continued, parallel investigation of controlled cognition in young adults as a possible model for age- or dementia-related declines in cognitive function and to determine if RT distribution parameters can truly be wed to functional neuroanatomy.

  22. Cognitive Control • Inhibition • Task Switching • Manipulation • Goal Maintenance A set of cognitive abilities that control and regulate other abilities and behaviors. “Span measures strongly predict a very broad range of higher-order cognitive capabilities, including language comprehension, reasoning and even general intelligence” Simon Task A “supervisory attention system” that is engaged during conflicts among task goals, external stimuli and well-learned response schemas ExecutiveFunction Automatic/Controlled Ospan ACC Young Adult Normal MCI AD Individual Differences PFC

  23. Acknowledgements • Janelle Seegmiller • Ann Lambert • Eve Miller • many CSL Research Assistants • Center on Aging Pilot Grant Program • Center for Alzheimer’s Care, Imaging, & Research • Drs. Norman Foster, Gordon Chelune, Jim Lee, Ed Hsu, & Sarang Joshi

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