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.
APOE ε 2 is associated with white matter hyperintensity volume in CADASIL / Gesierich, Benno; Opherk, Christian; Rosand, Jonathan; Gonik, Mariya; Malik, Rainer; Jouvent, Eric; Hervé, Dominique; Adib-Samii, Poneh; Bevan, Steve; Pianese, Luigi; Silvestri, Serena; Dotti, Maria T; De Stefano, Nicola; Van Der Grond, Jeroen; Boon, Elles M. J.; Pescini, Francesca; Rost, Natalia; Pantoni, Leonardo; Lesnik Oberstein, Saskia A.; Federico, Antonio; Ragno, Michele; Markus, Hugh S; Tournier-Lasserve, Elisabeth; Chabriat, Hugues; Dichgans, Martin; Duering, Marco; Ewers, Michael. - In: JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM. - ISSN 0271-678X. - ELETTRONICO. - 36:(2016), pp. 199-203. [10.1038/jcbfm.2015.85]
APOE ε 2 is associated with white matter hyperintensity volume in CADASIL
PESCINI, FRANCESCA;PANTONI, LEONARDO;
2016
Abstract
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.
I documenti in FLORE sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
