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血浆脂蛋白相关磷脂酶 A2(PLA2G7 V297F 缺失突变)遗传缺陷与日本阿尔茨海默病的风险。

Genetic deficiency of plasma lipoprotein-associated phospholipase A2 (PLA2G7 V297F null mutation) and risk of Alzheimer's disease in Japan.

机构信息

Genetics, GlaxoSmithKline, Research Triangle Park, NC 27709, USA.

出版信息

J Alzheimers Dis. 2010;21(3):775-80. doi: 10.3233/JAD-2010-100513.

Abstract

High plasma lipoprotein phospholipase A2 activity (Lp-PLA2) is reported to be a risk factor for dementia. A loss of function polymorphism in the Lp-PLA2 gene - PLA2G7 V279F - is found almost exclusively in Asians. In 1,952 subjects with late-onset AD and 2,079 non-demented controls recruited from Japan, the PLA2G7 null allele was not associated with risk or age at onset of AD: logistic regression OR 0.98 (95% CI 0.86-1.12, p=0.81) per additional null allele, adjusted for age/age at onset, gender, and APOE ε4. Genetic deficiency of Lp-PLA2 activity is not associated with a reduced risk of AD in the Japanese population.

摘要

高血浆脂蛋白磷脂酶 A2 活性(Lp-PLA2)被报道为痴呆的危险因素。Lp-PLA2 基因中的一种功能丧失性多态性 - PLA2G7 V279F - 几乎只存在于亚洲人群中。在从日本招募的 1952 名迟发性 AD 患者和 2079 名非痴呆对照者中,PLA2G7 无效等位基因与 AD 的风险或发病年龄无关:每增加一个无效等位基因,逻辑回归 OR 0.98(95%CI 0.86-1.12,p=0.81),调整年龄/发病年龄、性别和 APOE ε4。在日本人群中,Lp-PLA2 活性的遗传缺陷与 AD 风险降低无关。

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