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The association of Apolipoprotein E ε4 with symptomatic intracerebral hemorrhage, MRI markers and cognition in Dutch-type hereditary cerebral amyloid angiopathy
Journal article   Open access   Peer reviewed

The association of Apolipoprotein E ε4 with symptomatic intracerebral hemorrhage, MRI markers and cognition in Dutch-type hereditary cerebral amyloid angiopathy

Maaike C. van der Plas, Rosemarie van Dort, Ingeborg Rasing, Yongxi Long, Erik W. van Zwet, Matthias J.P. van Osch, Hamid R. Sohrabi, Kevin Taddei, Samantha L. Gardener, Ralph N. Martins, …
Journal of stroke and cerebrovascular diseases, Vol.35(4), 108593
2026
DOI: https://doi.org/10.1016/j.jstrokecerebrovasdis.2026.108593
PMID: 41707816
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Open Access CC BY V4.0

Abstract

Apolipoprotein E Cerebral amyloid angiopathy Intracerebral hemorrhage Stroke
Background Apolipoprotein E (APOE) genotype influences the presence, course and severity of sporadic cerebral amyloid angiopathy (sCAA). We investigated the effect of the APOE ε4-allele on clinical and neuroradiological outcomes in mutation-carriers with Dutch-type hereditary (D-)CAA. Methods Participants with D-CAA from a prospective cohort study, with data collected on history of symptomatic intracerebral hemorrhages (sICH) and vascular risk factors, underwent 3 Tesla magnetic resonance imaging (MRI) scans to assess macrobleeds, cerebral microbleeds (CMBs), cortical superficial siderosis (cSS), enlarged perivascular spaces (EPVS), white matter hyperintensity (WMH) volume and WMH multispot lesions. Global cognition was measured using Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) scores. Associations between ≥1 APOE ε4-allele and age of first sICH, time to recurrence, cognition and radiological data were analyzed with adjustments for confounders. Results Eighty-one participants (mean age 47 years, 54% women, 38% with sICH history) were included. The APOE ε4-allele was not associated with earlier sICH onset (median age 56 versus 57 years; p = 0.6) or time to recurrence (5.0 versus 3.9 years; p = 0.4), nor was it associated with macrobleeds (β 2.0; 95%CI 2.4- -2.7; p = 0.4), CMBs (β 2.9; 95%CI 1.0-8.9; p = 0.06), cSS (aOR 0.5; 95%CI 0.1-2.0; p = 0.3), EPVS (aOR 0.4; 95%CI 0.1-1.5; p = 0.6), WMH volume (β 6.8; 95%CI -1.9-15.4; p = ), a multispot pattern (OR 0.7; 95%CI 0.2-2.7, p = 0.6), or cognition (β -0.3; 95%CI -0.4- -0.5; p = 0.5). Conclusion APOE ε4 does not affect key clinical parameters or D-CAA neuroradiological markers and therefore does not explain the large variation in disease course in D-CAA.

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Citation topics
1 Clinical & Life Sciences
1.52 Neurodegenerative Diseases
1.52.60 Dementia
Web Of Science research areas
Neurosciences
Peripheral Vascular Disease
ESI research areas
Neuroscience & Behavior
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