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NEUROLOGY 2005;65:1666-1669
© 2005 American Academy of Neurology
Brief Communications

Increased incidence of genetic human prion disease in Hungary

G. G. Kovács, MD, PhD, L. László, PhD, A. Bakos, J. Minárovits, MD, PhD, DSc, M. T. Bishop, BSc, T. Ströbel, PhD, B. Vajna, PhD, E. Mitrova, MD, DSc and K. Majtényi, MD, PhD

From the National Institute of Psychiatry and Neurology (Drs. Kovács and Majtényi), Hungarian Reference Centre for Human Prion Disease; Departments of Anatomy, Cell and Development Biology (Dr. László) and Department of Microbiology (Dr. Vajna), Eötvös University; the Microbiological Research Group (A. Bakos and Dr. Minárovits), National Centre for Epidemiology, Budapest, Hungary; the National CJD Surveillance Unit (M. Bishop), University of Edinburgh, Western General Hospital, Edinburgh, UK; the Institute of Neurology (Dr. Ströbel), Medical University of Vienna and Austrian Reference Centre for Human Prion Disease, Austria; and the Institute of Preventative and Clinical Medicine (Dr. Mitrova), Slovak Medical University, National Reference Centre of Prion Diseases, Bratislava, Slovakia.

Address correspondence and reprint requests to Dr. Gábor G. Kovács, National Institute of Psychiatry and Neurology, Hungarian Reference Centre for Human Prion Disease, Hüvösvölgyi út 116, H-1021 Budapest, Hungary; e-mail: kovacsgg{at}opni.hu

The authors performed analysis of the prion protein gene (PRNP) in 27 out of 109 confirmed prion disease patients between 1994 and 2004. E200K mutation was found in 17 cases. Another 10 patients, lacking PRNP analysis, showed positive family history. The mean annual incidence (0.27/million) and proportion (25.6%) of genetic prion disease is unusually high in Hungary and might be related to the migration of ancestors from the Slovakian focus.

Supported by the Hungarian Ministry of Education, an EU-funded project SEEC-CJD (QLRT-2000-01441), and the Hungarian Ministry of Health (ETT 69/2003).

Disclosure: The authors report no conflicts of interest.

Received November 30, 2004. Accepted in final form August 15, 2005.




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