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  • Print publication year: 2017
  • Online publication date: May 2018

9 - Explicit Memory and Disease

Summary

Learning Objectives

  • • To describe the changes in brain anatomy and fMRI activity in patients with amnestic mild cognitive impairment.
  • • To identify the regions of the brain that atrophy in patients with early Alzheimer's disease and learn the proteins that are accumulated in these regions.
  • • To compare the behavioral performance and fMRI activations of mild traumatic brain injury patients and healthy control participants during working memory tasks.
  • • To understand how surgery on medial temporal lobe epilepsy patients has revealed associations between the left medial temporal lobe and the right medial temporal lobe and verbal long-term memory and visual long-term memory.
  • • To specify the location of the hippocampal lesion that causes transient global amnesia.
  • The previous chapters of this book have focused on the neural basis of memory in healthy adults. This chapter discusses five neurological diseases that affect the brain regions associated with explicit memory. Section 9.1 discusses patients with amnestic mild cognitive impairment. These patients have long-term memory deficits due to atrophy of medial temporal lobe regions including the hippocampus. Within a few years of being diagnosed with amnestic mild cognitive impairment, about half of these individuals are diagnosed with Alzheimer's disease, the topic of section 9.2. Patients with early Alzheimer's disease have more severe impairment of long-term memory and atrophy of the medial temporal lobe and the parietal lobe, two regions that have been associated with long-term memory (see Chapter 3). Alzheimer's disease patients also have abnormally high levels of proteins in the medial temporal lobe and the parietal lobe, which is thought to further disrupt processing in these regions. Section 9.3 focuses on patients with mild traumatic brain injury, who typically perform normally on working memory tasks but have increased fMRI activity within the dorsolateral prefrontal cortex and the parietal cortex, relative to healthy control participants. It is generally believed that such increases in fMRI activity reflect compensation, where these regions are recruited to perform normally on the task.

    Yassa, M. A., Stark, S. M., Bakker, A., Albert, M. S., Gallagher, M. & Stark, C. E. (2010). High-resolution structural and functional MRI of hippocampal CA3 and dentate gyrus in patients with amnestic Mild Cognitive Impairment. NeuroImage, 51, 1242–1252.
    Buckner, R. L., Snyder, A. Z., Shannon, B. J., LaRossa, G., Sachs, R., Fotenos, A. F., Sheline, Y. I., Klunk, W. E., Mathis, C. A., Morris, J. C. & Mintun, M. A. (2005). Molecular, structural, and functional characterization of Alzheimer's disease: Evidence for a relationship between default activity, amyloid, and memory. The Journal of Neuroscience, 25, 7709–7717.
    McAllister, T. W., Sparling, M. B., Flashman, L. A., Guerin, S. J., Mamourian, A. C. & Saykin, A. J. (2001). Differential working memory load effects after mild traumatic brain injury. NeuroImage, 14, 1004–1012.
    Jones-Gotman, M. (1986). Right hippocampal excision impairs learning and recall of a list of abstract designs. Neuropsychologia, 24, 659–670.
    Bartsch, T., Schönfeld, R., Müller, F. J., Alfke, K., Leplow, B., Aldenhoff, J., Deuschl, G. & Koch, J. M. (2010). Focal lesions of human hippocampal CA1 neurons in transient global amnesia impair place memory. Science, 328, 1412–1415.