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Living with Dementia

Functional Imaging

  • - Normal Aging & Dementia
  • Jun 25, 2011
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  • Viewed: 2665
Tags: | brewer | dat | dementia of the alzheimer type | emission computed tomography |

Saykin et al.  (1999)  employed functional magnetic resonance imaging to study semantic and episodic memory processing in a sample of patients with mild dementia of the Alzheimer type. During semantic memory tasks, both patients and controls activated inferior frontal regions,  particularly of the left hemisphere. The spatial extent of activation was increased in the group with DAT. Additional right frontal activation was observed in the patients with mild DAT. During an episodic memory (recognition) task, there was an absence of prefrontal activation in persons with DAT compared to controls, with greater activation in the medial temporal region than in controls. Together, these findings suggest that brain activation is not simply diminished as a function of DAT, but may also increase, and that spatial shifts in activation can occur. In fact, increased activation in inferior frontal brain regions subserving semantic memory that were directly related to the extent of local atrophy in persons with DAT have been reported (Johnson et al. 2000). Therefore, alterations in activation may be adaptive as a compensatory mechanism, a possibility that deserves further investigation using functional neuroimaging methods.  In another study, Saykin et al. (2000) correlated structure and function, and found that degree of hippocampal atrophy predicted frontal lobe activation during episodic memory.

Analyses of functional connectivity provide a new means of analyzing functional magnetic resonance imaging or positron emission tomography data to examine disruption in normal patterns of coactivation of brain regions within a functional circuitry (Friston et al. 1993). Antuono, Li, and Jones (2000) reported preliminary evidence of disrupted functional connectivity within the hippocampus of individuals with DAT. The degree of disruption of functional connectivity was greater than that in healthy controls, while persons with MCI had an intermediate level.

Event-related functional magnetic resonance imaging, a relatively new technique, permits comparison of brain activation patterns for each individual during successful performance of a task compared to unsuccessful performance (Brewer et al. 1998; Wagner et al. 1998). Using an event-related analysis of successful and unsuccessful performance, we found that healthy controls showed greater right medial temporal activation when listening to items they would later correctly recognize compared to items they did not remember (Saykin, et al. 1999). By contrast, persons with DAT failed to show the same degree of differential activity in this area.

A small number of studies have shown functional magnetic resonance imaging alterations in individuals at risk for dementia of the Alzheimer type. For example, Smith et al. (1999) showed diminished temporal fMRI activation during language tasks in individuals at risk for DAT.  Similarly,  Bookheimer et al. (2000) reported changes on fMRI in individuals at genetic risk for DAT.

In summary, resting state studies reveal lowered metabolism in association cortices, particularly in the temporoparietal region. Studies employing cognitive challenges during scanning have provided a complex pattern of findings, involving not only reduced activation, but also enlarged and shifted areas of activation in patients relative to controls. Whether the more widespread activation is due to a compensatory mechanism, a loss of inhibitory neural processing, or some other as yet unidentified process remains unanswered. Both structural and functional neuroimaging have provided rich insights into the neuroanatomic and neurophysiological changes in the brain in MCI and DAT. Future research integrating analyses of brain structure, brain activation patterns, and cognitive performance is likely to further illuminate brain-behavior relations and mechanisms of impairment and compensation in MCI and DAT.

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Laura A. Flashman, Ph.D.,
Heather A. Wishart, Ph.D.,
Thomas E. Oxman, M.D.,
and Andrew J. Saykin, Psy.D.

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REFERENCES

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  4. Kuhl, D.E., R.A. Koeppe, S. Minoshima, et al. 1999. In vivo mapping of cerebral acetylcholinesterase activity in aging and Alzheimer's disease. Neurology 52:691-99.
  5. Laakso, M.P., H. Soininen, K. Partanen, et al. 1995. Volumes of hippocampus, amygdala and frontal lobes in the MRI-based diagnosis of early Alzheimer's disease: correlation with memory functions. Journal of Neural Transmission, Parkinson Disease and Dementia Section 9 (1):73-86.
  6. Lange, K.W., B.J. Sahakian, N.P. Quinn, et al. 1995. Comparison of executive and visuospatial memory function in Huntington's disease and dementia of Alzheimer type matched for degree of dementia. Journal of Neurology, Neurosurgery, and Psychiatry 58 (5):598-606.
  7. Lauter, H. 1985. What do we know about Alzheimer's disease today? Danish Medical Bulletin 32 (Suppl. 1):S1-21.

Full References »

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