The apolipoprotein E ε4-allele and antihypertensive treatment are associated with increased risk of cerebral MRI white matter hyperintensities

被引:21
作者
Hogh, P.
Garde, E.
Mortensen, E. L.
Jorgensen, O. S.
Krabbe, K.
Waldemar, G.
机构
[1] Copenhagen Univ Hosp, Rigshosp, Ctr Neurosci, Dept Neurol,Memory Disorders Res Unit, DK-2100 Copenhagen, Denmark
[2] Copenhagen Univ Hosp, Rigshosp, Danish Res Ctr Magnet Resonance, Dept Pharmacol, DK-2100 Copenhagen, Denmark
[3] Copenhagen Univ Hosp, Dept Hlth Psychol, Hvidovre, Denmark
[4] Univ Copenhagen, Inst Publ Hlth, Copenhagen, Denmark
[5] Copenhagen Univ Hosp, Copenhagen Cty Ctr Prevent Med, Glostrup, Denmark
[6] Copenhagen Univ Hosp, Rigshosp, Lab Neuropsychiat, DK-2100 Copenhagen, Denmark
来源
ACTA NEUROLOGICA SCANDINAVICA | 2007年 / 115卷 / 04期
关键词
APOE; MRI; WMH; arterial hypertension; cerebrovascular;
D O I
10.1111/j.1600-0404.2006.00779.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective- Apolipoprotein E-epsilon 4 (APOE-epsilon 4) is a potential risk factor for cerebral vascular disease. The aim of the present study was to examine the relative importance of APOE-epsilon 4 and other relevant risk factors for the extent of cerebral white matter hyperintensity (WMH) in a community-based sample of elderly subjects. Methods- From a cohort of 976 subjects born in 1914, APOE genotype was determined and MRI examinations were carried out in 75 subjects. WMH were rated using a standard semi-quantitative method. ANOVA and regression analyses were conducted to explore the relative importance of the potential risk factors. Results- APOE genotype and antihypertensive treatment were significantly associated with severity of total WMH load (P < 0.05). Conclusions- The study confirmed the association between APOE-epsilon 4 and WMH. Pharmaceutical treatment for arterial hypertension was also associated with the total burden of WMH in this study.
引用
收藏
页码:248 / 253
页数:6
相关论文
共 47 条
[1]
Neurocardiovascular instability, hypotensive episodes, and MRI lesions in neurodegenerative dementia [J].
Ballard, C ;
O'Brien, J ;
Barber, B ;
Scheltens, P ;
Shaw, F ;
McKeith, I ;
Kenny, RA .
VASCULAR FACTORS IN ALZHEIMER'S DISEASE, 2000, 903 :442-445
[2]
White matter lesions on magnetic resonance imaging in dementia with Lewy bodies, Alzheimer's disease, vascular dementia, and normal aging [J].
Barber, R ;
Scheltens, F ;
Gholkar, A ;
Ballard, C ;
McKeith, I ;
Ince, P ;
Perry, R ;
O'Brien, J .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1999, 67 (01) :66-72
[3]
Apolipoprotein E ε4 allele, temporal lobe atrophy, and white matter lesions in late-life dementias [J].
Barber, R ;
Gholkar, A ;
Scheltens, P ;
Ballard, C ;
McKeith, IG ;
Morris, CM ;
O'Brien, JT .
ARCHIVES OF NEUROLOGY, 1999, 56 (08) :961-965
[4]
Apolipoprotein E ε4 allele is associated with vascular dementia [J].
Baum, Larry ;
Lam, Linda C. W. ;
Kwok, Timothy ;
Lee, Jenny ;
Chiu, Helen F. K. ;
Mok, Vincent C. T. ;
Wong, Adrian ;
Chen, Xiangyan ;
Cheung, Wing Sze ;
Pang, Chi Pui ;
Ma, Suk Ling ;
Tang, Nelson L. S. ;
Wong, Ka Sing .
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, 2006, 22 (04) :301-305
[5]
Bigler ED, 2000, AM J NEURORADIOL, V21, P1857
[6]
Carmelli D, 2000, J GERONTOL A-BIOL, V55, pM103
[7]
GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].
CORDER, EH ;
SAUNDERS, AM ;
STRITTMATTER, WJ ;
SCHMECHEL, DE ;
GASKELL, PC ;
SMALL, GW ;
ROSES, AD ;
HAINES, JL ;
PERICAKVANCE, MA .
SCIENCE, 1993, 261 (5123) :921-923
[8]
Interaction between hypertension, apoE, and cerebral white matter lesions [J].
de Leeuw, FE ;
Richard, F ;
de Groot, JC ;
van Duijn, CM ;
Hofman, A ;
van Gijn, J ;
Breteler, MMB .
STROKE, 2004, 35 (05) :1057-1060
[9]
Hypertension and cerebral white matter lesions in a prospective cohort study [J].
de Leeuw, FE ;
de Groot, JC ;
Oudkerk, M ;
Witteman, JCM ;
Hofman, A ;
van Gijn, J ;
Breteler, MMB .
BRAIN, 2002, 125 :765-772
[10]
Impact of apolipoprotein E ε4 and vascular disease on brain morphology in men from the NHLBI twin study [J].
DeCarli, C ;
Reed, T ;
Miller, BL ;
Wolf, PA ;
Swan, GE ;
Carmelli, D .
STROKE, 1999, 30 (08) :1548-1553