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NEUROLOGY 2006;67:710-712
© 2006 American Academy of Neurology


Brief Communications

CSF BACE1 activity is increased in CJD and Alzheimer disease versus other dementias

R.M.D. Holsinger, PhD, J. S. Lee, BSc, A. Boyd, Dip Gen Coun, C. L. Masters, MD and S. J. Collins, MD

From the University of Melbourne (R.M.D.H., J.S.L., A.B., C.L.M., S.J.C.), Parkville, Mental Health Research Institute of Victoria (R.M.D.H., C.L.M., S.J.C.), Parkville, and Australian National Creutzfeldt–Jakob Disease Registry (J.S.L., A.B., C.L.M., S.J.C.), Melbourne, Victoria, Australia.

Address correspondence and reprint requests to DrD. Holsinger, School of Biomedical Sciences, University of Sydney, Lidcombe, New South Wales, 1825, Australia, e-mail: d.holsinger{at}fhs.usyd.edu.au; or Dr. S.J. Collins, Department of Pathology, University of Melbourne, Parkville, Victoria, 3010, Australia, e-mail: stevenjc{at}unimelb.edu.au

To assess the diagnostic utility of CSF BACE1 activity for discriminating Alzheimer disease (AD) from other dementias, particularly Creutzfeldt–Jakob disease (CJD), the authors studied 26 patients with sporadic CJD, 21 patients with AD, and 21 patients with various non-AD, non-CJD dementias (DCs). CSF BACE1 activity was elevated in AD in comparison with DC (p = 0.01). Unexpectedly, CSF BACE1 activity was also increased in sporadic CJD (p = 0.02).


The Australian National CJD Registry is funded by the Commonwealth Department of Health and Ageing. R.M.D.H. is supported by an Early Career Researcher Grant from the University of Melbourne. This work was also supported in part by an Australian NHMRC Program Grant (no. 208978).

Disclosure: C.L. Masters is executive director and chair of the Scientific Advisory Board of Prana Biotechnology Ltd., a company aimed at providing therapeutic intervention for age-related diseases. The other authors declare no conflicts of interest.

Received December 23, 2005. Accepted in final form April 20, 2006.




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