THE APOLIPOPROTEIN-E EPSILON-2 ALLELE IS ASSOCIATED WITH AN INCREASED RISK OF EARLY-ONSET ALZHEIMERS-DISEASE AND A REDUCED SURVIVAL

被引：134

作者：

VANDUIJN, CM

DEKNIJFF, P

WEHNERT, A

DEVOECHT, J

BRONZOVA, JB

HAVEKES, LM

HOFMAN, A

VAN BROECKHOVEN, C

机构：

[1] UNIV ANTWERP, UIA, BORN BUNGE FDN, DEPT BIOCHEM, NEUROGENET LAB, B-2610 ANTWERP, BELGIUM

[2] ERASMUS UNIV ROTTERDAM, SCH MED, DEPT EPIDEMIOL & BIOSTAT, 3000 DR ROTTERDAM, NETHERLANDS

[3] TNO, INST PREVENT MED, GAUBIUS LAB, LEIDEN, NETHERLANDS

来源：

ANNALS OF NEUROLOGY | 1995年 / 37卷 / 05期

关键词：

D O I：

10.1002/ana.410370510

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

It was suggested that in contrast to the E4 allele, the E2 allele of the apolipoprotein E gene (APOE*2) has a protective effect for late-onset Alzheimer's disease and early-onset Alzheimer's disease (LOAD). We studied the role of the APOE*2 allele in the pathogenesis of EOAD in a Dutch population-based study of 175 probable LOAD patients with onset age at or before 65 years and 532 age-matched controls. In our population, there was no evidence for a protective effect of the APOE*2 allele on the risk of EOAD. However, our data show that among EOAD patients, survival for APOE*2 carriers was significantly reduced. When restricting the analysis to patients ascertained early after diagnosis at a stage of disease when mortality is low, our data suggest an increased risk of EOAD for subjects with APOE2E2, APOE2E3, APOE3E4, and APOE4E4 genotypes.

引用

页码：605 / 610

页数：6

共 32 条

[1] Das HK, McPherson J., Brun GAP, Et al., Isolation characterization, and mapping to chromosome 19 of the human apolipoprotein E gene, J Biol Chem, 260, pp. 6240-6247, (1985)
[2] Olaisen B., Teisberg P., Gedde-Dahl T., The locus for apolipoprotein E (apoE) is linked to the complement component C3 (C3) locus in chromosome 19 in man, Hum Genet, 62, pp. 233-236, (1982)
[3] Strittmatter WJ, Saunders AM, Schmechel D., Et al., Apolipoprotein E: high avidity binding to beta‐amyloid and increased frequency of type 4 allele in late‐onset familial Alzheimer's disease, Proc Natl Acad Sci USA, 90, pp. 1977-1981, (1993)
[4] Saunders AM, Strittmatter WJ, Schmechel D., Et al., Association of apolipoprotein E allele ε4 with late‐onset familial and sporadic Alzheimer's disease, Neurology, 43, pp. 1467-1472, (1993)
[5] Corder EH, Saunders AM, Strittmatter WJ, Et al., Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families, Science, 261, pp. 921-923, (1993)
[6] Chartier-Harlin MC, Parfitt M., Legrain S., Apolipoprotein E., Et al., E4 allele as a major risk factor for sporadic early and late‐onset form of Alzheimer's disease: analysis of the 19q13.2 chromosomal region, Human Molecular Genetics, 3, pp. 569-574, (1994)
[7] de van Duijn CM, Knijff P., Cruts M., Et al., Apolipoprotein E4 allele in a population‐based study of early‐onset Alzheimer's disease, Nature Genet, 7, pp. 74-78, (1994)
[8] Corder EH, Saunders AM, Risch NJ, Et al., Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease, Nature Genet, 7, pp. 180-184, (1994)
[9] West HL, Rebeck W., Hyman BT. Frequency of the apolipoprotein E ε2 allele is diminished in sporadic Alzheimer disease, Neurosci Lett, 175, pp. 46-48, (1994)
[10] Talbot C., Lendon C., Craddock N., Et al., Protection against Alzheimer's disease with apoE ε2, Lancet, 343, pp. 1432-1433, (1994)

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