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阿尔茨海默病大脑中与氧化损伤相关的微量元素失衡。

Imbalances of trace elements related to oxidative damage in Alzheimer's disease brain.

作者信息

Cornett C R, Markesbery W R, Ehmann W D

机构信息

Department of Chemistry, University of Kentucky, Lexington 40506-0055, USA.

出版信息

Neurotoxicology. 1998 Jun;19(3):339-45.

PMID:9621340
Abstract

Four elements that have been implicated in free-radical-induced oxidative stress in Alzheimer's disease (AD) were measured by instrumental neutron activation analysis (INAA) in seven brain regions from 58 AD patients and 21 control subjects. A statistically significant elevation of iron and zinc was observed in multiple regions of AD brain, compared with controls. Mercury was elevated in AD in most regions studied, but the high variability of mercury levels in both AD and control subjects prevented the AD-control difference from reaching significance. Selenium, a protective agent against mercury toxicity, was significantly elevated only in AD amygdala. The elevation of iron and zinc in AD brain has the potential of augmenting neuron degeneration through free radical processes.

摘要

通过仪器中子活化分析(INAA)对58例阿尔茨海默病(AD)患者和21例对照者的七个脑区进行检测,以测定与自由基诱导的氧化应激相关的四种元素。与对照组相比,AD患者脑内多个区域的铁和锌水平在统计学上显著升高。在所研究的大多数区域,AD患者脑内汞含量升高,但AD组和对照组汞水平的高度变异性使AD组与对照组之间的差异未达到显著水平。作为一种抗汞毒性的保护剂,硒仅在AD患者的杏仁核中显著升高。AD患者脑内铁和锌的升高有可能通过自由基过程加剧神经元变性。

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