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NEUROLOGY 2006;66:1770-1771
© 2006 American Academy of Neurology
Brief Communications

Tau protein hyperphosphorylation in sporadic ALS with cognitive impairment

M. J. Strong, MD, W. Yang, MD, W. L. Strong, BSc, C. Leystra-Lantz, BSc, H. Jaffe, PhD and H. C. Pant, PhD

From the Cell Biology Research Group (M.J.S., W.Y., W.L.S., C.L.-L.), Robart’s Research Institute, London, Ontario, Canada; Department of Clinical Neurological Sciences (M.J.S.), Schulich School of Medicine, The University of Western Ontario, London, Ontario, Canada; and National Institute of Neurological Disorders and Stroke (H.J., H.C.P.), National Institutes of Health, Bethesda, MD.

Address correspondence and reprint requests to Dr. Michael J. Strong, Room C7-120, UH-LHSC, London, Ontario, Canada, N6A 5A5; e-mail: mstrong{at}uwo.ca

The authors have characterized frontal cortical tau protein in cognitively intact (4) and cognitively impaired (ALSci, 4) ALS patients and compared it with control (2) or Alzheimer disease (AD, 1)- derived tau. The authors observed expression of both 3R and 4R tau isoforms; increased insoluble tau protein; phosphatase resistance; and hyperphosphorylation at T175, S208, and S210. Soluble tau from both AD and ALSci was also phosphorylated at S237. Tau hyperphosphorylation is associated with ALS.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the June 13 issue to find the title link for this article.

This research was supported by the ALS Society of Canada and ALSA.

Disclosure: The authors report no conflicts of interest.

Received September 16, 2005. Accepted in final form February 17, 2006.


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June 13 Highlights
Neurology 2006 66: 1616-1617. [Full Text] [PDF]



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