Age- and genotype-related neurophysiologic reactivity to oxidative stress in healthy adults.
Age- and genotype-related neurophysiologic reactivity to oxidative stress in healthy adults.
复制标题
健康成年人对氧化应激的年龄和基因型相关的神经生理反应。
DOI：
10.1016/j.neurobiolaging.2011.11.013
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发表时间：
2012
影响因子：
4.2
通讯作者：
Rogaev,EvgenyI
中科院分区：
文献类型：
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作者：
Ponomareva,NatalyaV;Goltsov,AndreyY;Kunijeva,SvetlanaS;Scheglova,NadejdaS;Malina,DariaD;Mitrofanov,AndreyA;Boikova,TatianaI;Rogaev,EvgenyI
载脂蛋白E基因（ApoE）的epsilon4等位基因以及衰老会增加患阿尔茨海默氏症和血管疾病的风险。脑电图（EEG）对过度通气（HV）的反应性取决于低碳酸血症引起的脑血管收缩，这可能在亚临床脑血管疾病患者中受损。125名健康受试者按ApoE基因型分层，分为年轻组（年龄28-50岁）和老年组（年龄51-82岁），静息和3分钟HV时定量脑电图。年轻ApoE-epsilon4携带者对HV的脑电反应性较强，表现为高电压δ波、θ波和尖峰波，且HV诱导的脑电相对功率变化大于年轻ApoE-epsilon4非携带者。脑电图对HV的反应性随着年龄的增长而下降，ApoE-epsilon4携带者比ApoE-epsilon4非携带者下降更明显。老年ApoE-epsilon4携带者与老年ApoE-epsilon4非携带者相比，hv诱导的脑电图相对功率变化较小。老年ApoE-epsilon4携带者脑电图对HV的反应性明显下降，提示血管因素可能影响apoe诱导的阿尔茨海默病的发病机制。
The epsilon4 allele of the apolipoprotein E gene (ApoE), as well as aging increase the risk of Alzheimer's and vascular diseases. Electroencephalogram (EEG) reactivity to hyperventilation (HV) depends on hypocapnia-induced cerebral vasoconstriction, which may be impaired in subjects with subclinical cerebrovascular disease. Quantitative EEG at rest and under 3-minute HV was examined in 125 healthy subjects divided into younger (age range 28–50) and older (age range 51–82) cohorts and stratified by ApoE genotype. The younger ApoE-epsilon4 carriers had excessive EEG reactivity to HV characterized by the manifestation of high-voltage delta, theta activity and sharp waves, and larger HV-induced changes in EEG relative powers than in the younger ApoE-epsilon4 noncarriers. EEG reactivity to HV decreased with aging, and in the ApoE-epsilon4 carriers the decrease was more pronounced than in the ApoE-epsilon4 noncarriers. The older ApoE-epsilon4 carriers had smaller HV-induced changes in EEG relative powers than the older ApoE-epsilon4 noncarriers. A marked decline of EEG reactivity to HV in the older ApoE-epsilon4 carriers suggests the possible impact of vascular factors on the pathogenesis of ApoE-induced Alzheimer disease.