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Updated: Jul 14, 2025

Using Retinal Imaging to Study Dementia
Published on: November 6, 2017
Intracranial arteriosclerosis and the risk of dementia: A population-based cohort study
Tim C van den Beukel1,2,3, Frank J Wolters1,4,5, Uwe Siebert6,7,8
1Department of Epidemiology, Erasmus Medical Center, Rotterdam, CA, The Netherlands.
Insights
Intracranial arteriosclerosis, including carotid and vertebrobasilar artery calcification, significantly elevates dementia risk. This link is partly explained by increased cerebral small vessel disease.
Area of Science:
- Neurology
- Vascular Medicine
- Gerontology
Background:
- The relationship between intracranial arteriosclerosis and dementia is not well understood.
- Arteriosclerosis affects blood vessels in the brain, potentially impacting cognitive function.
Purpose of the Study:
- To investigate the association between intracranial arteriosclerosis and dementia risk.
- To explore the mediating role of cerebral small vessel disease (cSVD) and brain structure volumes.
Main Methods:
- Assessed intracranial carotid artery calcification (ICAC) and vertebrobasilar artery calcification (VBAC) in 2339 dementia-free individuals.
- Utilized Cox models to analyze dementia risk and causal mediation analyses for indirect effects.
Main Results:
- Both ICAC presence and volume were associated with increased dementia risk (HR 1.53 and 1.19, respectively).
- Severe VBAC also increased dementia risk (HR 1.89).
- cSVD mediated 13% of the ICAC effect and 24% of the VBAC effect on dementia.
Conclusions:
- Intracranial arteriosclerosis is a significant risk factor for dementia.
- Cerebral small vessel disease partially mediates the link between intracranial arteriosclerosis and dementia.
Background:
The impact of intracranial arteriosclerosis on dementia remains largely unclear.
Methods:
In 2339 stroke-free and dementia-free participants (52.2% women, mean age 69.5 years) from the general population, we assessed intracranial carotid artery calcification (ICAC) and vertebrobasilar artery calcification (VBAC) as proxy for arteriosclerosis. Associations with dementia were assessed using Cox models. In addition, indirect effects through cerebral small vessel disease (cSVD) and subcortical brain structure volumes were assessed using causal mediation analyses.
Results:
During a median of 13.4 years (25th-75th percentiles 9.9-14.5) of follow-up, 282 participants developed dementia. Both ICAC presence (hazard ratio [HR]: 1.53, 95% confidence interval [CI]: 1.00-2.32]) and volume (HR per standard deviation: 1.19, 95% CI: 1.01-1.40) increased dementia risk. For VBAC, severe calcifications increased dementia risk (HR for third vs first volume tertile: 1.89, 95% CI: 1.00-3.59). These effects were mediated partly through increased cSVD (percentage mediated for ICAC: 13% and VBAC: 24%).
Discussion:
Intracranial arteriosclerosis increases the risk of dementia.
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