Intracranial arteriosclerosis is related to cerebral small vessel disease: a prospective cohort study

Elisabeth J. Vinke, Pinar Yilmaz, Janine E. van der Toorn, Rahman Fakhry, Kate Frenzen, Florian Dubost, Silvan Licher, Marleen de Bruijne, Maryam Kavousi, M. Arfan Ikram, Meike W. Vernooij, Daniel Bos*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

6 Citations (Scopus)


Intracranial arteriosclerosis has been increasingly recognized as a risk factor for cognitive impairment and even dementia. A possible mechanism linking intracranial arteriosclerosis to cognitive impairment and dementia involves structural brain changes including cerebral small vessel disease (CSVD). To assess whether intracranial carotid artery calcification (ICAC) and vertebrobasilar artery calcification (VBAC), as proxies for intracranial arteriosclerosis, are related to CSVD. Within the population-based Rotterdam Study, between 2003 and 2006 a computed tomography (CT)-based measurement of ICAC and VBAC and at least one magnetic resonance imaging (MRI) measurement of structural brain changes were performed from 2005 onwards in 1,489 participants. To estimate the burden of calcification independent of age, we computed age-adjusted percentile curves for ICAC and VBAC separately, based on the calcification volumes. Using the longitudinal MRI data, we assessed whether a larger calcification burden accelerates structural brain changes using appropriate statistical models for repeated outcome measures. A larger burden of ICAC and VBAC was associated with an increase of CSVD markers accelerating over time. A larger burden of ICAC and VBAC was not significantly (p > 0.05) associated with accelerated brain atrophy. Arteriosclerosis is related to accelerating structural brain changes over time.

Original languageEnglish
Pages (from-to)16-24
Number of pages9
JournalNeurobiology of Aging
Publication statusPublished - Sept 2021

Bibliographical note

Funding Information:
This study is part of the EuroPOND initiative, which is funded by the European Union's Horizon 2020 research and innovation programme under grant agreement No. 666992 . This project has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (project: ORACLE, grant agreement No: 678543 ). The Rotterdam Study is supported by Erasmus MC and Erasmus University Rotterdam; The Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development (ZonMw); the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture, and Science; the Ministry of Health, Welfare, and Sports; European Commission; and the Municipality of Rotterdam . Development of PVS quantification software was supported by The Netherlands Organisation for Health Research and Development (ZonMw) Project 104003005 and by Netherlands Organization for Scientific Research project VI.C.182.042. Dr. Bos was supported by a fellowship of the BrightFocus Foundation (A2017424F). None of the funders had any role in study design; study conduct; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the article.

Publisher Copyright:
© 2021


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