Oakley A E, Collingwood J F, Dobson J, Love G, Perrott H R, Edwardson J A, Elstner M, Morris C M
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK.
Neurology. 2007 May 22;68(21):1820-5. doi: 10.1212/01.wnl.0000262033.01945.9a.
Evidence suggests that abnormal iron metabolism is associated with Parkinson disease (PD), with raised iron levels found in pathologically affected areas in PD. It is unknown if this elevated iron is actually associated with neurons or reactive glia, and we therefore addressed this issue by determining if raised iron was present in single dopaminergic neurons.
We used unfixed frozen sections from postmortem tissue of PD patients and elderly normal individuals to avoid metal contamination and translocation. Levels of iron and other elements were measured using sensitive and specific wavelength dispersive electron probe x-ray microanalysis coupled with cathodoluminescence spectroscopy in individual substantia nigra dopaminergic neurons.
We identified raised intraneuronal iron in single defined substantia nigra neurons in PD (mean neuronal iron 2,838 vs 1,611, p < 0.0001) but not in other movement disorders such as Huntington disease. These findings were unrelated to the density of remaining neurons.
Primary changes in neuronal iron could lead to neurodegeneration in Parkinson disease.
有证据表明，铁代谢异常与帕金森病（PD）相关，在PD病理受累区域发现铁水平升高。目前尚不清楚这种升高的铁是否实际上与神经元或反应性胶质细胞有关，因此我们通过确定单个多巴胺能神经元中是否存在铁升高来解决这个问题。
我们使用PD患者和老年正常个体尸检组织的未固定冰冻切片，以避免金属污染和移位。在单个黑质多巴胺能神经元中，使用灵敏且特异的波长色散电子探针X射线微分析结合阴极发光光谱法测量铁和其他元素的水平。
我们在PD的单个明确的黑质神经元中发现神经元内铁升高（平均神经元铁含量为2838，而对照组为1611，p<0.0001），但在其他运动障碍如亨廷顿病中未发现。这些发现与剩余神经元的密度无关。
神经元铁的原发性变化可能导致帕金森病中的神经退行性变。
