Cerebral amyloid-β deposition in patients with heart disease or carotid occlusive disease: A systematic review and meta-analysis.
Autor: | Starmans NLP; Department of Neurology and Neurosurgery, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Electronic address: n.l.p.starmans@umcutrecht.nl., Leeuwis AE; Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, VU Medical Center, De Boelelaan 1117-1118, 1081 HV Amsterdam, the Netherlands., Biessels GJ; Department of Neurology and Neurosurgery, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands., Kappelle LJ; Department of Neurology and Neurosurgery, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands., van der Flier WM; Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam UMC, VU Medical Center, De Boelelaan 1117-1118, 1081 HV Amsterdam, the Netherlands; Department of Epidemiology, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117-1118, 1081 HV Amsterdam, the Netherlands., Tolboom N; Department of Radiology and Nuclear Medicine, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. |
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Jazyk: | angličtina |
Zdroj: | Journal of the neurological sciences [J Neurol Sci] 2023 Feb 15; Vol. 445, pp. 120551. Date of Electronic Publication: 2023 Jan 13. |
DOI: | 10.1016/j.jns.2023.120551 |
Abstrakt: | Background: Cardiovascular disease is an important contributor to cognitive impairment. This likely involves prototypical vascular disease mechanisms like ischemia, but cardiovascular disease might also impact the brain by accelerating cerebral amyloid-β accumulation. We aimed to determine whether there is an association between heart disease or carotid occlusive disease (COD) and cerebral amyloid-β burden. Methods: We conducted a systematic review of studies investigating cerebral amyloid-β burden, measured with positron emission tomography, in adults with and without heart disease or COD. Where possible, we obtained standardized mean differences (SMD) of amyloid-β standardized uptake volume ratios (SUVr) for meta-analysis. Results: Eight cross-sectional studies were identified (1478 participants, aged 60-81 years, 51% female). Three studies on heart disease (two on atrial fibrillation (AF) only, one on AF, coronary artery disease and heart failure) did not find a difference in amyloid-β burden between patients and controls. The pooled difference for 746 participants with and without AF did not reach significance (SMD SUVr 0.14, 95%CI -0.06-0.34). Of the five studies on COD (one on differences between participants with and without COD, four on differences between hemispheres in unilateral COD), four did not find a difference in amyloid-β between participants or hemispheres. The pooled difference in amyloid-β load between hemispheres in 24 patients with unilateral COD was not significant (SMD SUVr -0.13, 95%CI -0.70-0.43). Conclusion: Based on current studies, although limited and heterogeneous, there is insufficient evidence to support the hypothesis that heart disease or COD are associated with increased cerebral amyloid-β burden. Competing Interests: Declaration of Competing Interest None. (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.) |
Databáze: | MEDLINE |
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