Sökning: WFRF:(Brodtmann A.)
> (2016) >
Positron Emission T...
-
Sahathevan, R.
(författare)
Positron Emission Tomographic Imaging in Stroke Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke
- Artikel/kapitelEngelska2016
Förlag, utgivningsår, omfång ...
-
Ovid Technologies (Wolters Kluwer Health),2016
Nummerbeteckningar
-
LIBRIS-ID:oai:gup.ub.gu.se/230712
-
https://gup.ub.gu.se/publication/230712URI
-
https://doi.org/10.1161/strokeaha.115.010528DOI
Kompletterande språkuppgifter
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
Background and Purpose 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 -amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger -amyloid deposition, with deposition over time. Methods 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. Results Forty-seven patients were imaged with C-11-PiB positron emission tomography. There was an increase in C-11-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 C-11-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 C-11-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of C-11-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). Conclusions There was no significant increase in C-11-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric C-11-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased -amyloid deposition 18 months after stroke.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Lindén, Thomas,1962Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xlthol
(författare)
-
Villemagne, V. L.
(författare)
-
Churilov, L.
(författare)
-
Ly, J. V.
(författare)
-
Rowe, C.
(författare)
-
Donnan, G.
(författare)
-
Brodtmann, A.
(författare)
-
Göteborgs universitetInstitutionen för neurovetenskap och fysiologi
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Stroke: Ovid Technologies (Wolters Kluwer Health)47:1, s. 113-1190039-24991524-4628
Internetlänk
Hitta via bibliotek
-
Stroke
(Sök värdpublikationen i LIBRIS)
Till lärosätets databas