A Generalised Increase in Protein Carbonyls in the Brain in Parkinson's but Not Incidental Lewy Body Disease
Article first published online: 18 NOV 2002
Journal of Neurochemistry
Volume 69, Issue 3, pages 1326–1329, September 1997
How to Cite
Alam, Z. I., Daniel, S. E., Lees, A. J., Marsden, D. C., Jenner, P. and Halliwell, B. (1997), A Generalised Increase in Protein Carbonyls in the Brain in Parkinson's but Not Incidental Lewy Body Disease. Journal of Neurochemistry, 69: 1326–1329. doi: 10.1046/j.1471-4159.1997.69031326.x
- Issue published online: 18 NOV 2002
- Article first published online: 18 NOV 2002
- Resubmitted manuscript received June 13, 1997; accepted June 13, 1997.
- Parkinson's disease;
- Incidental Lewy body disease;
- Oxidative damage;
- Protein carbonyls
Abstract: The degeneration of neurones in Parkinson's disease (PD) may involve oxidative stress. Previously, increased lipid peroxidation and oxidative DNA damage have been reported in parkinsonian substantia nigra. In the present study the protein carbonyl assay was used to assess oxidative protein damage in postmortem brain tissue from patients with PD and age-matched controls. In brain areas associated with PD, such as substantia nigra, caudate nucleus, and putamen, there was a significant increase in carbonyl levels. However, increased carbonyl levels were also found in areas of the brain not thought to be affected in PD. This perhaps suggests that protein carbonyl formation is related to therapy with l-DOPA, which can exert prooxidant properties in vitro. Consistent with this possibility, brain regions from individuals with incidental Lewy body disease (putative presymptomatic PD) showed no rise in carbonyls in any brain areas. Our data show that either oxidative protein damage occurs widely but late in PD brain, and/or that l-DOPA treatment contributes to protein oxidation.