18F-Flutemetamol PET post-stroke - a seven year follow-up study

Abstract

Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or TIA without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or none. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In all, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding were not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed amyloid did not correlate with other measures related to neurodegeneration and cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

“…Stroke survivors were invited to participate in a follow-up study from February 2014 to July 2016. Details can be found in previous published papers (40,44).…”

Long term survival after a first transient ischaemic attack in England: A retrospective matched cohort study

“…A case-control study in Canada 8 reported HR=2.1 of composite death outcomes for cases relative to matched controls, and a PRISM study in Australia 16 reported a relative risk of death of 1.42. Some previous studies were often limited by small sample sizes [17][18] or short follow-up periods 19 . Furthermore, comparison of their results was limited due to methodological differences: prospective [16][17] versus retrospective follow-up 8,20 , the source of participants: hospital based 8,16 versus community based 15,18,21 , by stroke etiology, recruitment period and non-adjustment of confounding factors.…”