Frank Arne Wollenweber1, Sonja Därr1, Claudia Müller1, Marco Duering1, Katharina Buerger1, Vera Zietemann1, Rainer Malik1, Matthias Brendel1, Birgit Ertl-Wagner1, Peter Bartenstein1, Axel Rominger1, Martin Dichgans2. 1. From the Institute for Stroke and Dementia Research (F.A.W., C.M., M. Duering, K.B., V.Z., R.M., M. Dichgans), Department of Nuclear Medicine (S.D., M.B., P.B., A.R.), and Institute of Clinical Radiology (B.E.-W.), Klinikum der Universität München, Ludwig-Maximilians-Universität LMU, Munich, Germany; and German Center for Neurodegenerative Diseases (DZNE) (M. Dichgans) and Munich Cluster for Systems Neurology (SyNergy) (P.B., A.R., M. Dichgans), Germany. 2. From the Institute for Stroke and Dementia Research (F.A.W., C.M., M. Duering, K.B., V.Z., R.M., M. Dichgans), Department of Nuclear Medicine (S.D., M.B., P.B., A.R.), and Institute of Clinical Radiology (B.E.-W.), Klinikum der Universität München, Ludwig-Maximilians-Universität LMU, Munich, Germany; and German Center for Neurodegenerative Diseases (DZNE) (M. Dichgans) and Munich Cluster for Systems Neurology (SyNergy) (P.B., A.R., M. Dichgans), Germany. martin.dichgans@med.uni-muenchen.de.
Abstract
BACKGROUND AND PURPOSE: Mild cognitive impairment (MCI) is common after stroke and associated with poor outcome. However, the mechanisms underlying poststroke MCI (PS-MCI) are insufficiently understood. We performed amyloid-β positron emission tomography (PET) in a prospective cohort of stroke survivors to determine the role of amyloid pathology in PS-MCI. METHODS: We studied 178 consecutive patients enrolled into the prospective DEDEMAS study (Determinants of Dementia After Stroke). Follow-up visits 6 months post stroke included detailed cognitive testing, standardized magnetic resonance imaging, and amyloid-β imaging using flutemetamol ((18)F) PET. MCI was defined by the modified Petersen criteria. Amyloid-positivity was assessed visually and quantitatively. Fifty-six (31%) patients agreed to undergo PET imaging. RESULTS: Thirty-eight (68%) patients who consented to PET imaging had PS-MCI. Visual assessment revealed amyloid PET positivity in 2 (5%) of the 38 PS-MCI patients and in 2 (11%) of the 18 cognitively healthy stroke survivors. There was no correlation between flutemetamol ((18)F) standardized uptake value ratios and cognitive scores in the 56 patients. PS-MCI patients had significant cognitive impairments on executive function (P<0.01) and memory tests (P<0.01) when compared with cognitively healthy stroke survivors (P<0.01). CONCLUSIONS: The prevalence of amyloid-pathology in patients with PS-MCI is not increased when compared with cognitively healthy stroke survivors and to recent estimates for cognitively healthy elderly subjects. Factors other than amyloid-pathology likely contribute to the development of PS-MCI. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01334749.
BACKGROUND AND PURPOSE: Mild cognitive impairment (MCI) is common after stroke and associated with poor outcome. However, the mechanisms underlying poststroke MCI (PS-MCI) are insufficiently understood. We performed amyloid-β positron emission tomography (PET) in a prospective cohort of stroke survivors to determine the role of amyloid pathology in PS-MCI. METHODS: We studied 178 consecutive patients enrolled into the prospective DEDEMAS study (Determinants of Dementia After Stroke). Follow-up visits 6 months post stroke included detailed cognitive testing, standardized magnetic resonance imaging, and amyloid-β imaging using flutemetamol ((18)F) PET. MCI was defined by the modified Petersen criteria. Amyloid-positivity was assessed visually and quantitatively. Fifty-six (31%) patients agreed to undergo PET imaging. RESULTS: Thirty-eight (68%) patients who consented to PET imaging had PS-MCI. Visual assessment revealed amyloid PET positivity in 2 (5%) of the 38 PS-MCIpatients and in 2 (11%) of the 18 cognitively healthy stroke survivors. There was no correlation between flutemetamol ((18)F) standardized uptake value ratios and cognitive scores in the 56 patients. PS-MCIpatients had significant cognitive impairments on executive function (P<0.01) and memory tests (P<0.01) when compared with cognitively healthy stroke survivors (P<0.01). CONCLUSIONS: The prevalence of amyloid-pathology in patients with PS-MCI is not increased when compared with cognitively healthy stroke survivors and to recent estimates for cognitively healthy elderly subjects. Factors other than amyloid-pathology likely contribute to the development of PS-MCI. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01334749.