Salustri C, Tecchio F, Zappasodi F, Tomasevic L, Ercolani M, Moffa F, Cassetta E, Rossini P M, Squitti R
Institute of Cognitive Sciences and Technologies (CNR), Unità MEG, Fatebenefratelli Hospital, Isola Tiberina, 00186 Rome, Italy.
Institute of Cognitive Sciences and Technologies (CNR), Unità MEG, Fatebenefratelli Hospital, Isola Tiberina, 00186 Rome, Italy ; Department of Imaging, IRCCS San Raffaele Pisana, 00163 Rome, Italy.
Int J Alzheimers Dis. 2013;2013:638312. doi: 10.1155/2013/638312. Epub 2013 Dec 12.
Objective. To verify whether systemic biometals dysfunctions affect neurotransmission in living Alzheimer's disease (AD) patients. Methods. We performed a case-control study using magnetoencephalography to detect sensorimotor fields of AD patients, at rest and during median nerve stimulation. We analyzed position and amount of neurons synchronously activated by the stimulation in both hemispheres to investigate the capability of the primary somatosensory cortex to reorganize its circuitry disrupted by the disease. We also assessed systemic levels of copper, ceruloplasmin, non-Cp copper (i.e., copper not bound to ceruloplasmin), peroxides, transferrin, and total antioxidant capacity. Results. Patients' sensorimotor generators appeared spatially shifted, despite no change of latency and strength, while spontaneous activity sources appeared unchanged. Neuronal reorganization was greater in moderately ill patients, while delta activity increased in severe patients. Non-Cp copper was the only biological variable appearing to be associated with patient sensorimotor transmission. Conclusions. Our data strengthen the notion that non-Cp copper, not copper in general, affects neuronal activity in AD. Significance. High plasticity in the disease early stages in regions controlling more commonly used body parts strengthens the notion that physical and cognitive activities are protective factors against progression of dementia.
目的。验证全身性生物金属功能障碍是否会影响活体阿尔茨海默病(AD)患者的神经传递。方法。我们进行了一项病例对照研究,使用脑磁图来检测AD患者在静息状态和正中神经刺激期间的感觉运动区。我们分析了双侧半球中由刺激同步激活的神经元的位置和数量,以研究初级体感皮层重组其被疾病破坏的神经回路的能力。我们还评估了铜、铜蓝蛋白、非铜蓝蛋白结合铜(即未与铜蓝蛋白结合的铜)、过氧化物、转铁蛋白和总抗氧化能力的全身水平。结果。患者的感觉运动发生器在空间上出现了移位,尽管潜伏期和强度没有变化,而自发活动源则没有改变。中度患病患者的神经元重组更为明显,而重度患者的δ活动增加。非铜蓝蛋白结合铜是唯一似乎与患者感觉运动传递相关的生物学变量。结论。我们的数据强化了这样一种观念,即影响AD神经元活动的是非铜蓝蛋白结合铜,而非一般意义上的铜。意义。在疾病早期,控制更常用身体部位的区域具有高可塑性,这强化了身体和认知活动是预防痴呆进展的保护因素这一观念。