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Nature Medicine 14, 711 - 712 (2008)
doi:10.1038/nm0708-711

Regulatory RNA goes awry in Alzheimer's disease

Peter St George-Hyslop1 & Christian Haass2

  1. Peter St. George-Hyslop is in the Department of Clinical Neurosciences, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK. He is also in the Department of Medicine, University of Toronto, Toronto Western Hospital and Centre for Research in Neurodegenerative Diseases, 6 Queens Park Crescent, Toronto, Ontario M5S 3H2, Canada.
    e-mail: phs22@cam.ac.uk
  2. Christian Haass is at the Center for Integrated Protein Science Munich and Adolf-Butenandt-Institute, Department of Biochemistry, Laboratory for Neurodegenerative Disease Research, Schillerstrasse 44, Ludwig-Maximilians-University, 80336 Munich, Germany.


An antisense RNA may contribute to Alzheimer's disease by upregulating beta-secretase (pages 723–730).


In the current issue of Nature Medicine, Faghihi et al.1 report that a noncoding antisense RNA against beta-secretase, also known as BACE1 (beta-site amyloid precursor protein (APP)-cleaving enzyme), may contribute to pathogenesis of Alzheimer's disease. BACE1 is a vertebrate-specific enzyme, which, together with presenilin-dependent gamma-secretase, cleaves APP to generate the neurotoxic amyloid-beta peptide (Abeta).

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