Iron level changes in the brain with neurodegenerative disease

Q3 Engineering
Robert Bazala , Giorgio Zoppellaro , Gunther Kletetschka
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Abstract

Nanosized magnetite inside ferritin may control the progression of neurodegenerative disease (ND) by creating an electronic noise in the neural cells. We discovered that brains with ND have a unique electron paramagnetic resonance (EPR) spectrum. Our measurements showed that the collapse of the broad ferritin maximum contained in the EPR spectra possibly relates to the onset and progression of the ND. Ferritin malfunction triggers the perturbation of iron concentration that either increases or decreases over the normal levels in brain without ND. This supports a conjecture that accumulated iron results in an increased volume of magnetite crystals, whose fluctuated magnetic moments may interfere with the normal function of neural synapses and contribute to the neurodegenerative disease. The mechanism of the iron mobility relates to iron canals in the neural cell's membrane by which the iron enters and leaves the neural cells. This gate keeper malfunction may relate to a speculation that this is due to the appearance of 2Fe-2S in EPR spectra of brains with ND.

Statement of significance

In this manuscript we describe feedback between electronic structure of atoms in the brain, easiness of becoming magnetized in a magnetic field and the ability of the brain to hold the magnetic field on its own in cases of neurodegenerative-diseased and healthy brain. This contribution is novel and significant for a number of reasons, as follows: We revealed that diseased brains have a distinct electronic structure from healthy brains. We identified the easiness of brain samples to become magnetized in a magnetic field and the brains’ ability to hold the magnetic field on its own in cases of neurodegenerative-diseased and healthy brains. This paper addresses a new hypothesis, and we consider that it will generate broad that may be of broad interdisciplinary interest and generate further debate.

神经退行性疾病患者大脑铁水平的变化
铁蛋白内的纳米磁铁矿可能通过在神经细胞中产生电子噪声来控制神经退行性疾病(ND)的进展。我们发现患有ND的大脑具有独特的电子顺磁共振(EPR)谱。我们的测量表明,EPR光谱中宽铁蛋白最大值的崩溃可能与ND的发生和发展有关。铁蛋白功能障碍会引起铁浓度的紊乱,在没有ND的大脑中,铁浓度会高于或低于正常水平。这支持了一种推测,即铁的积累导致磁铁矿晶体体积的增加,磁铁矿晶体的磁矩波动可能干扰神经突触的正常功能,并导致神经退行性疾病。铁离子迁移的机制与神经细胞膜上的铁通道有关,铁离子通过这些通道进出神经细胞。这种闸门管理员故障可能与一种推测有关,即这是由于ND脑的EPR光谱中出现2Fe-2S所致。在这篇论文中,我们描述了在神经退行性疾病和健康大脑的情况下,大脑中原子的电子结构、在磁场中被磁化的容易程度和大脑自身保持磁场的能力之间的反馈。这一贡献是新颖而重要的,原因如下:我们揭示了患病大脑与健康大脑具有不同的电子结构。我们确定了大脑样本在磁场中被磁化的容易程度,以及大脑在神经退行性疾病和健康大脑的情况下自己保持磁场的能力。这篇论文提出了一个新的假设,我们认为它将产生广泛的跨学科兴趣,并产生进一步的辩论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Brain multiphysics
Brain multiphysics Physics and Astronomy (General), Modelling and Simulation, Neuroscience (General), Biomedical Engineering
CiteScore
4.80
自引率
0.00%
发文量
0
审稿时长
68 days
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