Surowka Artur Dawid, Wrobel Pawel, Adamek Dariusz, Radwanska Edyta, Szczerbowska-Boruchowska Magdalena
AGH University of Science and Technology, Faculty of Physics and Applied Computer Science, al. A. Mickiewicza 30, 30-059 Krakow, Poland.
Metallomics. 2015 Nov;7(11):1522-31. doi: 10.1039/c5mt00154d. Epub 2015 Oct 6.
Human brain aging is considered to be the leading risk factor for a variety of neurodegenerative alterations. In particular, it is thought that the human substantia nigra might play a pivotal role in age-associated dopamine depletion which could be responsible for neuronal demise and subsequent emergence of different neurological alterations. A plethora of neurochemical redox- and non-redox-driven mechanisms is mainly associated with modifications in the elemental composition of both neuromelanin-pigmented neurons and extraneuronal spaces in the human substantia nigra pars compacta (SNpc). An age-associated variation in the content of Fe, Cu, Zn and Ca has recently received great interest in neurology, as these elements are implicated in different biochemical mechanisms underlying malicious neurodegenerative disorders, including Parkinson's and Alzheimer's diseases. Interestingly, to the best our knowledge, there is lack of a comprehensive study on age-associated variation in the elemental composition of the human SNpc. In that respect, the aim of the present study was to make a preliminary attempt to unravel some of the age-associated mechanisms responsible for the metabolism of some redox-active and redox-inactive elements in the elderly. To do so, substantia nigra tissue specimens, drawn from 37 individuals who deceased without any signs of neurodegeneration, were subjected to spectroscopic studies using synchrotron radiation based X-ray fluorescence. Both neuromelanin-pigmented neurons and extraneuronal areas were studied. It appears that in the neurons, Fe tends to decrease, whilst Cu, Zn and Ca were found to accumulate as an individual gets older.
人类大脑衰老被认为是多种神经退行性改变的主要风险因素。特别是，人们认为人类黑质可能在与年龄相关的多巴胺耗竭中起关键作用，而多巴胺耗竭可能导致神经元死亡以及随后出现不同的神经学改变。大量由神经化学氧化还原和非氧化还原驱动的机制主要与人类致密部黑质（SNpc）中神经黑色素色素神经元和神经外间隙的元素组成变化有关。最近，铁、铜、锌和钙含量的年龄相关变化在神经学领域引起了极大关注，因为这些元素与包括帕金森病和阿尔茨海默病在内的恶性神经退行性疾病背后的不同生化机制有关。有趣的是，据我们所知，目前还缺乏关于人类SNpc元素组成年龄相关变化的全面研究。在这方面，本研究的目的是初步尝试揭示一些与老年人某些氧化还原活性和非氧化还原活性元素代谢相关的年龄相关机制。为此，从37名无任何神经退行性病变迹象的死者身上获取黑质组织标本，使用基于同步辐射的X射线荧光进行光谱研究。对神经黑色素色素神经元和神经外区域都进行了研究。结果显示，在神经元中，随着个体年龄的增长，铁含量趋于下降，而铜、锌和钙含量则会积累。
