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APOE and Cerebral Small Vessel Disease Markers in Patients With Intracerebral Hemorrhage



Hostettler, Isabel Charlotte;

Seiffge, David;

Wong, Andrew;

Ambler, Gareth;

Wilson, Duncan;

Shakeshaft, Clare;

Banerjee, Gargi;

Werring, David J; + view all

Hostettler, Isabel Charlotte;

Seiffge, David;

Wong, Andrew;

Ambler, Gareth;

Wilson, Duncan;

Shakeshaft, Clare;

Banerjee, Gargi;

Sharma, Nikhil;

Jäger, Hans Rolf;

Cohen, Hannah;

Yousry, Tarek A;

Al-Shahi Salman, Rustam;

Lip, Gregory YH;

Brown, Martin M;

Muir, Keith;

Houlden, Henry;

Werring, David J;

– view fewer

(2022)

APOE and Cerebral Small Vessel Disease Markers in Patients With Intracerebral Hemorrhage.

Neurology
, 99
(12)

e1290-e1298.

10.1212/WNL.0000000000200851.


Text

Banerjee_Complete_manuscript_ApoE_10022022_clean_2.pdf

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Abstract

BACKGROUND AND OBJECTIVE: We investigated the associations between the APOE genotype, intracerebral hemorrhage (ICH), and neuroimaging markers of cerebral amyloid angiopathy (CAA). METHODS: We included patients from a prospective, multicenter UK observational cohort study of patients with ICH and representative UK population controls. First, we assessed the association of the APOE genotype with ICH (compared with controls without ICH). Second, among patients with ICH, we assessed the association of APOE status with the hematoma location (lobar or deep) and brain CT markers of CAA (finger-like projections [FLP] and subarachnoid extension [SAE]). RESULTS: We included 907 patients with ICH and 2,636 controls. The mean age was 73.2 (12.4 SD) years for ICH cases vs 69.6 (0.2 SD) for population controls; 50.3% of cases and 42.1% of controls were female. Compared with controls, any APOE ε2 allele was associated with all ICH (lobar and nonlobar) and lobar ICH on its own in the dominant model (OR 1.38, 95% CI 1.13-1.7, p = 0.002 and OR 1.50, 95% CI 1.1-2.04, p = 0.01, respectively) but not deep ICH in an age-adjusted analyses (OR 1.26, 95% CI 0.97-1.63, p = 0.08). In the cases-only analysis, the APOE ε4 allele was associated with lobar compared with deep ICH in an age-adjusted analyses (OR 1.56, 95% CI 1.1-2.2, p = 0.01). When assessing CAA markers, APOE alleles were independently associated with FLP (ε4: OR 1.74, 95% CI 1.04-2.93, p = 0.04 and ε2/ε4: 2.56, 95% CI 0.99-6.61, p = 0.05). We did not find an association between APOE alleles and SAE. DISCUSSION: We confirmed associations between APOE alleles and ICH including lobar ICH. Our analysis shows selective associations between APOE ε2 and ε4 alleles with FLP, a CT marker of CAA. Our findings suggest that different APOE alleles might have diverging influences on individual neuroimaging biomarkers of CAA-associated ICH.

Type: Article

Title: APOE and Cerebral Small Vessel Disease Markers in Patients With Intracerebral Hemorrhage
Location: United States
DOI: 10.1212/WNL.0000000000200851
Publisher version: https://doi.org/10.1212/WNL.0000000000200851
Language: English
Additional information: This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
Keywords: Aged, Apolipoprotein E2, Apolipoprotein E4, Biomarkers, Cerebral Amyloid Angiopathy, Cerebral Hemorrhage, Cerebral Small Vessel Diseases, Female, Humans, Male, Prospective Studies
UCL classification: UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Department of Neuromuscular Diseases
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science > Population Science and Experimental Medicine > MRC Unit for Lifelong Hlth and Ageing
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science > Population Science and Experimental Medicine
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Brain Repair and Rehabilitation
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Haematology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Institute of Prion Diseases
URI: https://discovery.ucl.ac.uk/id/eprint/10156489
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