Positron Emission Tomographic Imaging in Stroke Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke

So if there was β-amyloid accumulation in the stroke area what difference would it make if that area is dead? Or were they trying to say it was located in the penumbra? If this didn't find anything why exactly is there an increased risk of dementia/Alzheimers after a stroke?
http://stroke.ahajournals.org/content/47/1/113.full?

1. Ramesh Sahathevan, PhD;
2. Thomas Linden, PhD;
3. Victor L. Villemagne, MD;
4. Leonid Churilov, PhD;
5. John V. Ly;
6. Christopher Rowe, MD;
7. Geoffrey Donnan, MD*;
8. Amy Brodtmann, PhD*

+ Author Affiliations

1. From the Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia (R.S., T.L., L.C., J.V.L., G.D., A.D.); University of Melbourne, Victoria, Australia (R.S., V.L.V., L.C., J.V.L., C.R., G.D., A.D.); Universiti Kebangsaan Malaysia Medical Centre, Bangi, Malaysia (R.S.); Gothenburg University, Gothenburg, Sweden (T.L.); and Austin Hospital PET Centre, Melbourne, Victoria, Australia (V.L.V., C.R.).

1. Correspondence to Amy Brodtmann, PhD, Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, 245 Burgundy St, Heidelberg, Victoria 3081, Australia. E-mail agbrod@unimelb.edu.au

1. ↵* Drs Donnan and Brodtmann contributed equally.

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Abstract

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 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.

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 ¹¹C-PiB positron emission tomography. There was an increase in ¹¹C-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 ¹¹C-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 ¹¹C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of ¹¹C-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 ¹¹C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric ¹¹C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ≤18 months after stroke.