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Prevalence of Amyloid Positron Emission Tomographic Positivity in Poststroke Mild Cognitive Impairment
Frank Arne Wollenweber1, Sonja Därr1, Claudia Müller1
1From 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.
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.
Insights
Amyloid pathology is not more common in stroke survivors with mild cognitive impairment (MCI). Other factors likely cause PS-MCI, suggesting new research directions for post-stroke cognitive decline.
Area of Science:
- Neurology
- Neuroimaging
- Cognitive Science
Background:
- Mild cognitive impairment (MCI) frequently occurs after stroke, impacting patient outcomes.
- The underlying mechanisms of post-stroke MCI (PS-MCI) remain poorly understood.
- Amyloid pathology is a potential contributor to cognitive decline.
Purpose of the Study:
- To investigate the role of amyloid-beta (Aβ) pathology in the development of PS-MCI.
- To assess Aβ deposition in stroke survivors using positron emission tomography (PET).
Main Methods:
- Prospective cohort study (DEDEMAS) of 178 stroke survivors.
- Cognitive testing, MRI, and amyloid-β PET imaging with flutemetamol (18F) at 6 months post-stroke.
- MCI diagnosis using modified Petersen criteria; amyloid-positivity assessed visually and quantitatively.
Main Results:
- Of 56 patients undergoing PET, 38 (68%) had PS-MCI.
- Amyloid PET positivity was low in both PS-MCI (2/38) and cognitively healthy (2/18) groups.
- No correlation found between amyloid uptake and cognitive scores; PS-MCI patients showed executive function and memory deficits.
Conclusions:
- Amyloid pathology prevalence in PS-MCI is not elevated compared to controls.
- Factors beyond amyloid pathology likely drive PS-MCI development.
- Further research is needed to identify other contributors to cognitive impairment after stroke.
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