No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study
Stroke
Cognitive Decline
Neurochemistry
Amyloid (mycology)
DOI:
10.1186/s12883-020-01753-w
Publication Date:
2020-05-08T10:02:58Z
AUTHORS (11)
ABSTRACT
Abstract Background Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI unclear. We hypothesize that deposition, measured Flutemetamol ( 18 F-Flut) positron emission tomography (PET), common seven-year survivors diagnosed and, further, quantitatively assessed F-Flut-PET uptake 7 years correlates amyloid-β peptide (Aβ 42 ) levels cerebrospinal fluid (CSF) at 1 year, measures neurodegeneration cognition post-stroke. Methods 208 patients first-ever or transient Ischemic Attack (TIA) without pre-existing were included during 2007 2008. At one- seven-years post-stroke, cognitive status was assessed, categorized into dementia, mild normal. Etiologic sub-classification based on magnetic resonance imaging (MRI) findings, CSF biomarkers clinical profile. years, offered F-Flut-PET, amyloid-positivity visually semi-quantitatively. associations between standardized value ratios (SUVr) (medial temporal lobe atrophy (MTLA), global cortical (GCA)) (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) Aβ using linear regression. Results In total, 111 completed 7-year follow-up, 26 agreed to PET imaging, whom 13 had from year. Thirteen out but only one positivity. MTA grade, GCA scale, MMSE score TMT-A did not correlate SUVr this cohort. Conclusions Amyloid binding CI. Quantitatively deposition other related cognition. Therefore, may be a key mediator Trial registration Clinicaltrials.gov NCT00506818 ). July 23, 2007. Inclusion February 2007, randomization intervention May trial
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