Iron and Aluminum Increase in the Substantia Nigra of Patients with Parkinson's Disease: An X-Ray Microanalysis
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 56, Issue 2, pages 446–451, February 1991
How to Cite
Hirsch, E. C., Brandel, J.-P., Galle, P., Javoy-Agid, F. and Agid, Y. (1991), Iron and Aluminum Increase in the Substantia Nigra of Patients with Parkinson's Disease: An X-Ray Microanalysis. Journal of Neurochemistry, 56: 446–451. doi: 10.1111/j.1471-4159.1991.tb08170.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received March 2, 1990; revised manuscript received July 13, 1990; accepted July 19, 1990.
- Parkinson's disease;
- Cell death;
- Substantia nigra;
Abstract: The levels of different elements were studied by x-ray microanalysis in the substantia nigra and the central gray substance of patients with Parkinson's disease, progressive supranuclear palsy, and matched controls. In control brains, only iron, potassium, silicium, sodium, sulfur, and zinc were within the limit of detection of the technique. The abundance of each element was different, but their respective concentrations in the two brain regions were similar, except for sulfur levels which were higher on neuromelanin aggregates in the substantia nigra than in nigral regions lacking neuromelanin, and in the central gray substance. In Parkinson's disease, but not in progressive supranuclear palsy, nigral iron levels increased in regions devoid of neuromelanin and decreased on neuromelanin aggregates, but were unchanged in the central gray substance, when compared to control values. Concentrations of the other elements in the central gray substance and substantia nigra were not different from controls in brains from patients with Parkinson's disease and progressive supranuclear palsy. Analysis of Lewy bodies in the parkinsonian substantia nigra revealed high levels of iron and the presence of aluminum. Metal abundance was not affected in progressive supranuclear palsy, in spite of the nigral cell death. This suggests that the increased iron levels and the detection of aluminum observed in Parkinson's disease are not solely the consequence of the neuronal degeneration.