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|Title:||Positron Emission Tomographic Imaging in Stroke: Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke.|
|Authors:||Sahathevan, Ramesh;Linden, Thomas;Villemagne, Victor L;Churilov, Leonid;Ly, John V;Rowe, Christopher C;Donnan, Geoffrey A;Brodtmann, Amy|
|Affiliation:||Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia|
University of Melbourne, Victoria, Australia
Universiti Kebangsaan Malaysia Medical Centre, Bangi, Malaysia
Gothenburg University, Gothenburg, Sweden
The Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia
|Citation:||Stroke 2016; 47(1): 113-119|
|Abstract:||Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction-driving amyloid deposition. We conducted a study to determine the presence of β-amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger β-amyloid deposition, with deposition over time. Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup ≤18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration. Forty-seven patients were imaged with (11)C-PiB positron emission tomography. There was an increase in (11)C-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, -0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of (11)C-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, -0.02 to 0.10]; P=0.095). We repeated (11)C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of (11)C-PiB between regions of interest (median difference in standardized uptake value ratio, -0.08 [95% confidence interval, -0.23 to -0.03]; P=0.04). There was no significant increase in (11)C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric (11)C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ≤18 months after stroke.|
Research Support, Non-U.S. Gov't
positron emission tomography
|Appears in Collections:||Journal articles|
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