Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/18629
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
Issue Date: Jan-2016
EDate: 2015-11-17
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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/18629
DOI: 10.1161/STROKEAHA.115.010528
ORCID: 0000-0003-3910-2453
PubMed URL: 26578658
Type: Journal Article
Research Support, Non-U.S. Gov't
Subjects: Alzheimer disease
follow-up studies
positron emission tomography
risk factors
Appears in Collections:Journal articles

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