Neurology
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Neurology 2002;59:137-138
© 2002 American Academy of Neurology
Brief Communications

Brain aconitase activity is not decreased in progressive supranuclear palsy

P. S. Fitzmaurice, PhD, C. L. Bamsey, MSc, L. Ang, MD, M. Guttman, MD, A. H. Rajput, MD, Y. Furukawa, MD and S. J. Kish, PhD

From the Human Neurochemical Pathology Laboratory (Drs. Fitzmaurice, Guttman, and Kish, and C. Bamsey), and Movement Disorders Research Laboratory (Dr. Furukawa), Centre for Addiction and Mental Health, Toronto, Ontario; Division of Neurology (Dr. Rajput), University of Saskatchewan, Saskatoon, Saskatchewan; and Division of Neuropathology (Dr. Ang), London Health Science Centre, University of Western Ontario, London, Ontario, Canada.

Address correspondence and reprint requests to Paul Fitzmaurice, PhD, Human Neurochemical Pathology Section, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario, Canada M5T 1R8.

The novel finding of decreased activity of aconitase, a key Krebs cycle enzyme highly sensitive to oxidative damage, in cybrid cell lines using mitochondrial DNA from patients with progressive supranuclear palsy (PSP) implies an enzyme abnormality in brain. However, the authors found that postmortem brain aconitase activity is normal in PSP. This suggests that patients with PSP do not have systemic aconitase deficiency and that data derived from cybrid cell models of neurodegenerative disorders might not always predict similar changes in human brain.






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