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Burden of Dilated Perivascular Spaces, an Emerging Marker of Cerebral Small Vessel Disease, Is Highly Heritable

Duperron, Marie-Gabrielle and Tzourio, Christophe and Sargurupremraj, Muralidharan and Mazoyer, Bernard and Soumare, Aicha and Schilling, Sabrina and Amouyel, Philippe and Chauhan, Ganesh and Zhu, Yi-Cheng and Debette, Stephanie (2018) Burden of Dilated Perivascular Spaces, an Emerging Marker of Cerebral Small Vessel Disease, Is Highly Heritable. In: STROKE, 49 (2). pp. 282-287.

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Official URL: http://dx.doi.org/10.1161/STROKEAHA.117.019309

Abstract

Background and Purpose-The genetic contribution to dilated perivascular space (dPVS) burden-an emerging MRI marker of cerebral small vessel disease-is unknown. We measured the heritability of dPVS burden and its shared heritability with other MRI markers of cerebral small vessel disease. Methods-The study sample comprised 1597 participants from the population-based Three City (3C) Dijon Study, with brain MRI and genome-wide genotyping (mean age, 72.8 +/- 4.1 years; 61% women). dPVS burden and lacunar brain infarcts were rated on a semiquantitative scale, whereas an automated algorithm generated white matter hyperintensity volume (WMHV). We estimated dPVS burden heritability and shared heritability with WMHV and lacunar brain infarcts using the genome-wide complex trait analysis tool, on unrelated participants, adjusting for age, sex, intracranial volume, and principal components of population stratification. Results-dPVS burden was significantly correlated with WMHV and lacunar brain infarcts, the strongest correlation being found between WMHV and dPVS in basal ganglia. Heritability estimates were h(2) = 0.59 +/- 0.24 (P = 0.007) for dPVS burden, h(2) = 0.54 +/- 0.24 (P = 0.010) for WMHV, and h(2) = 0.48 +/- 0.81 (P = 0.278) for lacunar brain infarcts. We found a nonsignificant trend toward shared heritability between dPVS and WMHV (r(g) = 0.41 +/- 0.28; P = 0.096), which seemed driven by dPVS in basal ganglia (r(g) = 0.72 +/- 0.61; P= 0.126) and not dPVS in white matter (r(g) =-0.10 +/- 0.36; P = 0.393). A genetic risk score for WMHV based on published loci was associated with increased dPVS burden in basal ganglia (P = 0.031). Conclusions-We provide evidence for important genetic contribution to dPVS burden in older community-dwelling people, some of which may be shared with WMHV. Differential heritability patterns for dPVS in white matter and basal ganglia suggest at least partly distinct underlying biological processes.

Item Type: Journal Article
Additional Information: Copy right for this article belong to the LIPPINCOTT WILLIAMS & WILKINS, TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
Department/Centre: Autonomous Societies / Centres > Centre for Brain Research
Depositing User: Id for Latest eprints
Date Deposited: 02 Mar 2018 15:05
Last Modified: 01 Feb 2019 09:26
URI: http://eprints.iisc.ac.in/id/eprint/58906

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