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Sökning: WFRF:(Brodtmann A.)

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  • Sachdev, P. S., et al. (författare)
  • STROKOG (stroke and cognition consortium): An international consortium to examine the epidemiology, diagnosis, and treatment of neurocognitive disorders in relation to cerebrovascular disease
  • 2017
  • Ingår i: Alzheimer's & Dementia. - 1552-5260 .- 1552-5279. ; 7, s. 11-23
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction The Stroke and Cognition consortium (STROKOG) aims to facilitate a better understanding of the determinants of vascular contributions to cognitive disorders and help improve the diagnosis and treatment of vascular cognitive disorders (VCD). Methods Longitudinal studies with ≥75 participants who had suffered or were at risk of stroke or TIA and which evaluated cognitive function were invited to join STROKOG. The consortium will facilitate projects investigating rates and patterns of cognitive decline, risk factors for VCD, and biomarkers of vascular dementia. Results Currently, STROKOG includes 25 (21 published) studies, with 12,092 participants from five continents. The duration of follow-up ranges from 3 months to 21 years. Discussion Although data harmonization will be a key challenge, STROKOG is in a unique position to reuse and combine international cohort data and fully explore patient level characteristics and outcomes. STROKOG could potentially transform our understanding of VCD and have a worldwide impact on promoting better vascular cognitive outcomes. © 2016 The Authors
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  • Lo, J. W., et al. (författare)
  • Profile of and risk factors for poststroke cognitive impairment in diverse ethnoregional groups
  • 2019
  • Ingår i: Neurology. - 0028-3878. ; 93:24, s. E2257-E2271
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective To address the variability in prevalence estimates and inconsistencies in potential risk factors for poststroke cognitive impairment (PSCI) using a standardized approach and individual participant data (IPD) from international cohorts in the Stroke and Cognition Consortium (STROKOG) consortium. Methods We harmonized data from 13 studies based in 8 countries. Neuropsychological test scores 2 to 6 months after stroke or TIA and appropriate normative data were used to calculate standardized cognitive domain scores. Domain-specific impairment was based on percentile cutoffs from normative groups, and associations between domain scores and risk factors were examined with 1-stage IPD meta-analysis. Results In a combined sample of 3,146 participants admitted to hospital for stroke (97%) or TIA (3%), 44% were impaired in global cognition and 30% to 35% were impaired in individual domains 2 to 6 months after the index event. Diabetes mellitus and a history of stroke were strongly associated with poorer cognitive function after covariate adjustments; hypertension, smoking, and atrial fibrillation had weaker domain-specific associations. While there were no significant differences in domain impairment among ethnoracial groups, some interethnic differences were found in the effects of risk factors on cognition. Conclusions This study confirms the high prevalence of PSCI in diverse populations, highlights common risk factors, in particular diabetes mellitus, and points to ethnoracial differences that warrant attention in the development of prevention strategies.
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  • Sahathevan, R., et al. (författare)
  • Positron Emission Tomographic Imaging in Stroke Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke
  • 2016
  • Ingår i: Stroke. - 0039-2499. ; 47:1, s. 113-119
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Purpose Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction-driving amyloid deposition. We conducted a study to determine the presence of -amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger -amyloid deposition, with deposition over time. Methods Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup 18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration. Results Forty-seven patients were imaged with C-11-PiB positron emission tomography. There was an increase in C-11-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, -0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of C-11-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, -0.02 to 0.10]; P=0.095). We repeated C-11-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of C-11-PiB between regions of interest (median difference in standardized uptake value ratio, -0.08 [95% confidence interval, -0.23 to -0.03]; P=0.04). Conclusions There was no significant increase in C-11-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric C-11-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased -amyloid deposition 18 months after stroke.
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