Bevelacqua J J, Mortazavi S M J
Bevelacqua Resources, 343 Adair Drive, Richland, WA 99352, USA.
Biophotonics Lab, Department of Electrical Engineering, University of Wisconsin Milwaukee, 3200 N Cramer St., Milwaukee, WI 53211, USA.
J Biomed Phys Eng. 2018 Jun 1;8(2):153-156. eCollection 2018 Jun.
In 2016, scientists reported that human exposure to low doses of ionizing radiation (CT scans of the brain) might relieve symptoms of both Alzheimer's disease (AD) and Parkinson disease (PD). The findings were unbelievable for those who were not familiar with neurohormesis. X-ray stimulation of the patient's adaptive protection systems against neurodegenerative diseases was the mechanism proposed by those authors. Now, some more recent studies performed in the field of neurobiological research confirm that low levels of stress can produce protective responses against the pathogenic processes. This paper outlines possible protective consequences of LDR in preventing the pathogenesis of AD through mechanisms such as restoring the myelin sheath and preventing neurodegeneration caused by oxidative stress. Focal demyelination is frequently reported in the proximity of beta-amyloid plaques within neocortex. Extracellular accumulation of amyloid is among well-characterized pathological changes in AD. It should be noted that LDR has been shown to contribute to the regeneration and functional recovery after transverse peripheral nerve injury (through inducing increased production of VEGF and GAP-43), which advances both the axonal regeneration and myelination. Another mechanism which is possibly involved is preventing neurodegeneration caused by oxidative stress. While high doses can induce reactive oxygen species (ROS) formation, oxidative stress and neuro-inflammation, substantial evidence now indicates that LDR can mitigate tissue damage through antioxidant defenses. Although adult neurogenesis has been reported to be beneficial for the regeneration of nervous system, some studies demonstrate that neurogenesis increases in AD brains. In spite of these reports, cellular therapy is introduced as a promising strategy for AD, and hence, LDR can affect the proliferation and differentiation of neural stem cells. Although such mechanisms are not fully known yet, it is hoped that this paper would foster further investigation into the mechanisms of this phenomenon, which accordingly improves human health.
2016年,科学家报告称,人类暴露于低剂量电离辐射(脑部CT扫描)可能会缓解阿尔茨海默病(AD)和帕金森病(PD)的症状。对于那些不熟悉神经激素效应的人来说,这些发现令人难以置信。这些作者提出的机制是,通过X射线刺激患者针对神经退行性疾病的适应性保护系统。现在,神经生物学研究领域进行的一些最新研究证实,低水平的应激可以产生针对致病过程的保护反应。本文概述了低剂量辐射(LDR)通过恢复髓鞘和预防氧化应激引起的神经退行性变等机制,在预防AD发病机制中可能产生的保护作用。在新皮质内β-淀粉样斑块附近经常报告有局灶性脱髓鞘。淀粉样蛋白的细胞外积累是AD中特征明确的病理变化之一。应该注意的是,低剂量辐射已被证明有助于周围神经横断损伤后的再生和功能恢复(通过诱导VEGF和GAP-43产量增加),这促进了轴突再生和髓鞘形成。另一个可能涉及的机制是预防氧化应激引起的神经退行性变。虽然高剂量可诱导活性氧(ROS)形成、氧化应激和神经炎症,但现在大量证据表明,低剂量辐射可通过抗氧化防御减轻组织损伤。虽然据报道成年神经发生对神经系统的再生有益,但一些研究表明AD大脑中的神经发生会增加。尽管有这些报道,但细胞疗法作为一种有前景的AD治疗策略被引入,因此,低剂量辐射可影响神经干细胞的增殖和分化。虽然这些机制尚未完全清楚,但希望本文能促进对这一现象机制的进一步研究,从而改善人类健康。