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Apolipoprotein(a) null phenotype is related to a delayed age at onset of Alzheimer's disease

被引：12
作者：
Emanuele, E
Peros, E
Tomaino, C
Feudatari, E
Bernardi, L
Binetti, G
Maletta, R
D'Angelo, A
Montagna, L
Bruni, AC
Geroldi, D
机构：
[1] IRCCS Policlin San Matteo, Mol Med Lab, I-27100 Pavia, Italy
[2] Univ Pavia, IRCCS Policlin San Matteo, Dept Internal Med & Med Therapeut, I-27100 Pavia, Italy
[3] Reg Ctr Neurogenet, Lamezia Terme, CZ, Italy
[4] IRCCS Ctr San Giovanni Dio, Memory Clin & Neurobiol Lab, Brescia, Italy
来源：
NEUROSCIENCE LETTERS | 2004年 / 357卷 / 01期
关键词：
Alzheimer's disease; apolipoprotein(a); null phenotype; age at onset; apolipoproteinE epsilon 4 allele; independent association;
D O I：
10.1016/j.neulet.2003.12.043
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Apolipoprotein(a) [apo(a)] is a highly polymorphic glycoprotein which has been suggested to play a role in Alzheimer's disease (AD). Plasma lipoprotein(a) [Lp(a)] levels and the differential expression of apo(a) isoforms were analyzed in 73 sporadic AD patients compared with 73 age- and gender-matched healthy controls. The distribution of apo(a) isoforms and Lp(a) concentrations were similar in the two groups. However, we observed that AD patients with no apo(a) isoform from immunoblots (subjects with the 'null phenotype') had a mean age at onset of 76.8 +/- 8.8 versus 66.9 +/- 9.6 years of those who expressed at least one apo(a) band (P = 0.010). Multivariate analysis showed that this effect was independent of apolipoproteinE epsilon4 allele. We conclude that the expression of at least one apo(a) isoform may interact with other pathogenic mechanisms involved in controlling the age at onset of AD. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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收藏
页码：45 / 48
页数：4
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