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Article type: Research Article
Authors: Rogaeva, Ekaterinaa; b | Kawarai, Toshitakaa | George-Hyslop, Peter Sta; b; c; *
Affiliations: [a] Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto, 6 Queen's Park Crescent West, Toronto, ON, Canada M5S 3H2 | [b] Department of Medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada | [c] Toronto Western Hospital Research Institute, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada
Correspondence: [*] Corresponding author: Peter St George-Hyslop, Centre for Neurodegenerative Diseases, Department of Medicine, University of Toronto, 6 Queen's Park Crescent West, Toronto, OO, Canada, M5S 3H2. Tel.: +1 416 946 7927; Fax: +1 416 978 1878; E-mail: p.hyslop@utoronto.ca.
Abstract: About 1% of Alzheimer's Disease (AD) cases have an early-onset autosomal dominant familial form of the disease, genetic analyses of which have found three causal genes: amyloid β-protein precursor (AβPP), presenilin 1 (PS1) and presenilin 2 (PS2). The APOE gene is the only robustly replicated risk factor for the common form of AD with onset after 65 years of age. In at least half of the AD cases, there is no known cause of the disease. Here we provide an overview on known AD-linked genes and discuss the strategies of searching for novel AD genetic risk factors.
Keywords: Alzheimer's disease, presenilin, gene, AβPP, APOE
DOI: 10.3233/JAD-2006-9S343
Journal: Journal of Alzheimer's Disease, vol. 9, no. s3, pp. 381-387, 2006
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