Qualitative changes in human ?-secretase underlie familial Alzheimer's disease


Por: Szaruga M., Veugelen S., Benurwar M., Lismont S., Sepulveda-Falla D., Lleo A., Ryan N.S., Lashley T., Fox N.C., Murayama S., Gijsen H., De Strooper B., Chávez-Gutiérrez L.

Publicada: 1 ene 2015
Resumen:
Presenilin (PSEN) pathogenic mutations cause familial Alzheimer's disease (AD [FAD]) in an autosomal-dominant manner. The extent to which the healthy and diseased alleles influence each other to cause neurodegeneration remains unclear. In this study, we assessed ?-secretase activity in brain samples from 15 nondemented subjects, 22 FAD patients harboring nine different mutations in PSEN1, and 11 sporadic AD (SAD) patients. FAD and control brain samples had similar overall ?-secretase activity levels, and therefore, loss of overall (endopeptidase) ?-secretase function cannot be an essential part of the pathogenic mechanism. In contrast, impaired carboxypeptidase-like activity (?-secretase dysfunction) is a constant feature in all FAD brains. Significantly, we demonstrate that pharmacological activation of the carboxypeptidase-like ?-secretase activity with ?-secretase modulators alleviates the mutant PSEN pathogenic effects. Most SAD cases display normal endo- and carboxypeptidase- like ?-secretase activities. However and interestingly, a few SAD patient samples display ?-secretase dysfunction, suggesting that ?-secretase may play a role in some SAD cases. In conclusion, our study highlights qualitative shifts in amyloid-ß (Aß) profiles as the common denominator in FAD and supports a model in which the healthy allele contributes with normal Aß products and the diseased allele generates longer aggregation-prone peptides that act as seeds inducing toxic amyloid conformations. © 2015 Szaruga et al.

Filiaciones:
Szaruga M.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium

Veugelen S.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium

Benurwar M.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium

Lismont S.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium

Sepulveda-Falla D.:
 Institut für Neuropathologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, 20246, Germany

 Neuroscience Group of Antioquia, Faculty of Medicine, University of Antioquia, Medellín, 1226, Colombia

Lleo A.:
 Unidad de Memoria, Departamento de Neurología, Institut d'Investigacions Biomèdiques Sant Pau, Hospital de Sant Pau, Barcelona, 08025, Spain

 Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Madrid, 28049, Spain

Ryan N.S.:
 Dementia Research Centre, University College London, London, WC1N 3AR, United Kingdom

Lashley T.:
 Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, University College London, London, WC1N 3AR, United Kingdom

Fox N.C.:
 Dementia Research Centre, University College London, London, WC1N 3AR, United Kingdom

Murayama S.:
 Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, 173-0015, Japan

Gijsen H.:
 Janssen Research and Development Division, Janssen Pharmaceutica NV, Beerse, 2340, Belgium

De Strooper B.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium

 Department of Molecular Neuroscience, Institute of Neurology, University College London, London, WC1N 3AR, United Kingdom

Chávez-Gutiérrez L.:
 VIB Center for the Biology of Disease, University of Leuven, KU Leuven, Leuven, 3000, Belgium

 Center for Human Genetics (CME), Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven (KU Leuven), Leuven, 3000, Belgium
ISSN: 00221007
Editorial
Rockefeller University Press, 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 212 Número: 12
Páginas: 2003-2013
WOS Id: 000368248200006
ID de PubMed: 26481686
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