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NEUROLOGY 2004;63:364-366
© 2004 American Academy of Neurology
Brief Communications

Prion protein codon 129 polymorphism and risk of Alzheimer disease

M. Riemenschneider, MD, N. Klopp, PhD, W. Xiang, PhD, S. Wagenpfeil, PhD, C. Vollmert, PhD, U. Müller, MD, H. Förstl, MD, T. Illig, PhD, H. Kretzschmar, MD and A. Kurz, MD

From the Neurochemistry and Neurogenetics Laboratory (Dr. Riemenschneider), Department of Psychiatry and Psychotherapy (Drs. Förstl and Kurz), and Department of Medical Statistics and Epidemiology (Dr. Wagenpfeil), Technische Universität Munich, Institute of Epidemiology (Drs. Klopp, Vollmert, and Illig) and Genome Analysis Center (Drs. Klopp and Illig), GSF Research Center for Environment and Health, Munich–Neuherberg, Department of Neuropathology (Drs. Xiang and Kretzschmar), Ludwig Maximilians Universität München, and Institute of Human Genetics (Dr. Müller), University of Giessen, Germany.

Address correspondence and reprint requests to Dr. M. Riemenschneider, Neurochemistry and Neurogenetics Laboratory, Department of Psychiatry and Psychotherapy, Technische Universität München, Ismaningerstr. 22, 81675 Munich, Germany; e-mail: m.riemenschneider{at}lrz.tu-muenchen.de

The authors investigated the PRNP Met129Val polymorphism in 1,393 subjects including 482 patients with Alzheimer disease (AD) and two independent control groups. In patients, PRNP Met homozygosity conferred increasing risk with decreasing age at onset (onset: 61 to 70 years, n = 151, p = 0.02, odds ratio [OR] = 1.72, 95% CI = 1.2 to 2.53; onset: ≤60 years, n = 138, p = 0.013, OR = 1.92, 95% CI = 1.31 to 2.87), whereas no association was obtained in patients with onset at older than 70 years. The results suggest involvement of the prion protein in the pathogenesis of early-onset AD.

Received November 14, 2003. Accepted in final form March 11, 2004.




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