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.
Full text not available from this repository. (Request a copy)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 |
|---|---|
| Publication: | STROKE |
| 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 |
| 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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