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No evidence for amy...
No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke : a seven-year follow-up study
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- Hagberg, Guri (författare)
- Bærum Hospital, Vestre Viken Hospital Trust, Drammen, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway
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- Ihle-Hansen, Hege (författare)
- Bærum Hospital, Vestre Viken Hospital Trust, Drammen, Norway; Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway
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- Fure, Brynjar, 1959- (författare)
- Region Örebro län,Örebro universitet, Institutionen för medicinska vetenskaper,Department of Neurology, Department of Internal Medicine, Central Hospital Karlstad, Karlstad, Sweden
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- Thommessen, Bente (författare)
- Department of Neurology, Akershus University Hospital, Oslo, Norway
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- Ihle-Hansen, Håkon (författare)
- Bærum Hospital, Vestre Viken Hospital Trust, Drammen, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway
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- Øksengård, Anne Rita (författare)
- Bærum Hospital, Vestre Viken Hospital Trust, Drammen, Norway
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- Beyer, Mona K. (författare)
- Division of Radiology, Nuclear Medicine Oslo University Hospital, Oslo, Norway
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- Wyller, Torgeir B. (författare)
- Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway
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- Müller, Ebba Gløersen (författare)
- Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Nuclear Medicine, Oslo University Hospital, Oslo, Norway
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- Pendlebury, Sarah T. (författare)
- Centre for Prevention of Stroke and Dementia, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK; NIHR Oxford Biomedical Research Centre, John Radcliffe Hospital, Oxford, UK
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- Selnes, Per (författare)
- Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Neurology, Akershus University Hospital, Oslo, Norway
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(creator_code:org_t)
- 2020-05-08
- 2020
- Engelska.
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Ingår i: BMC Neurology. - : BioMed Central. - 1471-2377. ; 20:1
- Relaterad länk:
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https://doi.org/10.1...
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https://bmcneurol.bi...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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 (F-18-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed F-18-Flut-PET uptake after 7 years correlates with amyloid-beta peptide (A beta(42)) levels in cerebrospinal fluid (CSF) at 1 year, and with measures of neurodegeneration and cognition at 7 years post-stroke.Methods: 208 patients with first-ever stroke or transient Ischemic Attack (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 normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At 7 years, patients were offered F-18-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between F-18-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 A beta(42) levels were assessed using linear regression.Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from 1 year. Thirteen out of 26 patients were diagnosed with CI 7 years post-stroke, but only one had visually assessed amyloid positivity. CSF A beta(42) levels at 1 year, MTA grade, GCA scale, MMSE score or TMT-A at 7 years did not correlate with F-18-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration 7 years post-stroke.Trial registration: Clinicaltrials.gov(NCT00506818). July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Neurologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Neurology (hsv//eng)
Nyckelord
- Cerebrospinal fluid
- Cognitive impairment
- Positron emission tomography
- Prognosis
- Stroke
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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- Av författaren/redakt...
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Hagberg, Guri
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Ihle-Hansen, Heg ...
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Fure, Brynjar, 1 ...
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Thommessen, Bent ...
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Ihle-Hansen, Håk ...
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Øksengård, Anne ...
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visa fler...
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Beyer, Mona K.
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Wyller, Torgeir ...
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Müller, Ebba Glø ...
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Pendlebury, Sara ...
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Selnes, Per
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BMC Neurology
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Örebro universitet