APOE ɛ2 is associated with white matter hyperintensity volume in CADASIL
Author(s) -
Benno Gesierich,
Christian Opherk,
Jonathan Rosand,
Mariya Gonik,
Rainer Malik,
Éric Jouvent,
Dominique Hervé,
Poneh AdibSamii,
Steve Bevan,
Luigi Pianese,
Serena Silvestri,
Maria Teresa Dotti,
Nicola De Stefano,
Jeroen van der Grond,
Elles M. J. Boon,
Francesca Pescini,
Natalia S. Rost,
Leonardo Pantoni,
Saskia A.J. Lesnik Oberstein,
Antonio Federico,
Michele Ragno,
Hugh S. Markus,
Elisabeth TournierLasserve,
Hugues Chabriat,
Martin Dichgans,
Marco Duering,
Michael Ewers
Publication year - 2015
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.2015.85
Subject(s) - cadasil , apolipoprotein e , cerebral amyloid angiopathy , leukoencephalopathy , hyperintensity , white matter , medicine , pathology , angiopathy , magnetic resonance imaging , disease , dementia , endocrinology , radiology , diabetes mellitus
Apolipoprotein E (APOE) increases the risk for Alzheimer’s disease (ɛ4 allele) and cerebral amyloid angiopathy (ɛ2 and ɛ4), but its role in small vessel disease (SVD) is debated. Here we studied the effects of APOE on white matter hyperintensity volume (WMHV) in CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), a nonamyloidogenic angiopathy and inherited early-onset form of pure SVD. Four hundred and eighty-eight subjects were recruited through a multicenter consortium. Compared with APOE ɛ3/ɛ3, WMHV was increased in APOE ɛ2 (P = 0.02) but not APOE ɛ4. The results remained significant when controlled for genome-wide genetic background variation. Our findings suggest a modifying influence of APOE ɛ2 on WMHV caused by pure SVD.
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