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首页 » 生物研究 » Journal of Alzheimer's Disease:PM2.5伤大脑?空气污染物增加患阿兹海默症风险

Journal of Alzheimer's Disease:PM2.5伤大脑?空气污染物增加患阿兹海默症风险

来源:生物谷 2015-02-05 13:10

2015年2月5日讯 /生物谷BIOON/-- 墨西哥蒙大拿大学(Universities of Montana)研究人员联合其他研究所的学者在最近一期的Journal of Alzheimer's Disease发表了一篇研究结果。他们发现携带载脂蛋白E(apolipoprotein E,APOE) ε4等位基因的儿童如果暴露在空气污染物之下(包括PM2.5),出现认知记忆方面的减退,患老年痴呆的风险会有所增加。

APOEε4等位基因是最常见的阿兹海默症遗传风险基因。不过空气污染物与阿兹海默症之间的关系的却很少有人注意。而墨西哥城是一个快速发展伴随严重环境污染的城市,800万城市生活的儿童都不得不每天暴露在PM2.5超标的环境中。为了评估APOEε4健康儿童在认知,嗅觉和代谢性脑指数方面是否受到空气污染物影响,研究人员对50个生活在墨西哥城市的13.4±4.8岁携带APOEε3或者APOEε4的孩子进行了韦氏儿童智力量表(WISC-R)评分和气味鉴别实验,同时用质子磁共振测量海马,脑桥,额叶顶叶白质的脑代谢产物。如预测一样,携带APOEε4的孩子右额叶白质的关键代谢产物比例比APOEε3的儿童要少,对肥皂的臭味鉴别困难,言语和智商平分低于平均分,并且显现出短期记忆和对关注的显著递减。 

研究人员认为是持续暴露于城市空气污染造成的认知不佳,胶质细胞和神经元代谢的改变。居住在严重污染的城市,APOEε4的综合影响可能导致神经退行性变化的加速。空气污染是一个严重的公共卫生问题,暴露于空气中污染物的浓度达到或超过现行标准已经被证实与神经炎症和神经病理学相关。在美国,有2亿人居住在臭氧和细颗粒物污染物超标的环境中。而且已经有证据显示颗粒污染物与因中风,心血管和呼吸系统疾病的死亡率增加有明显关系。而生活在像墨西哥大城市儿童的相关的健康问题更多。

目前迫切需要有一个更深入的研究证明APOEε4和空气污染的相互作用能影响儿童的大脑,或许将来能提供对阿尔茨海默氏病的预防前所未有的新提示。(生物谷Bioon.com)

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DOI: 10.3233/JAD-142685

 Decreases in Short Term Memory, IQ, and Altered Brain Metabolic Ratios in Urban Apolipoprotein ε 4 Children Exposed to Air Pollution

Lilian Calderon-Garcidueňas, Antonieta Mora-Tiscareňo, Maricela Franco-Lira, Hongtu Zhu, Zhaohua Lu, Edelmira Solorio, Ricardo Torres-Jardón and Amedeo D'Angiulli

Abstract

Children's urban air pollution exposures result in systemic and brain inflammation and the early hallmarks of Alzheimer's disease (AD). The apolipoprotein E (APOE) ε4 allele is the most prevalent genetic risk for AD. We assessed whether APOE in healthy children modulates cognition, olfaction, and metabolic brain indices. The Wechsler Intelligence Scale for Children (WISC-R) and the University of Pennsylvania Smell Identification Test were administered to 50 Mexico City Metropolitan Area children (13.4 ± 4.8 years, 28 APOE ε3 and 22 APOE ε4). N-acetylaspartate (NAA)/creatine (Cr), choline (Cho)/Cr, myo-inositol (mI)/Cr, and NAA/mI were calculated using proton magnetic resonance spectroscopy in the white matter of the frontal and parietal lobes, hippocampus, and pons. APOE ε4 versus ε3 children had a reduced NAA/Cr ratio in the right frontal white matter and decrements on attention, short-term memory, and below-average scores in Verbal and Full Scale IQ (>10 points). APOE modulated the group effects between WISC-R and left frontal and parietal white matter, and hippocampus metabolites. Soap was the predominantly failed odor AD-related item in urban children and in APOE ε4 versus ε3 carriers strongly correlated with left hippocampus mI/Cr ratio. APOE modulates responses to air pollution on the developing brain. APOE ε4 carriers could have a higher risk of developing early AD if they reside in a polluted environment. APOE, cognition, and olfaction testing and targeted magnetic resonance spectroscopy may contribute to the assessment of urban children and their results could provide new paths toward the unprecedented opportunity for early neuroprotection and AD prevention.

 
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