Journal article
Welcome to the complex disease world
Experimental neurology, v 184(1), pp 50-53
Nov 2003
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The recent explosion in our understanding of Alzheimer's disease (AD) at both the molecular and biochemical levels is due, in large part, to the successful utilization of genetic and genomic analyses over the past two decades. Initial positional cloning efforts of the 80s and 90s led to the identification of three genes, amyloid precursor protein (APP) and presenilins 1 and 2 (PSEN1 and PSEN2), that can harbor mutations leading to the rare, early-onset (<60 years) familial form of AD. Phenotypically, the majority of these early-onset mutations (>150 in total; a complete list of early-onset AD mutations can be found at the Alzheimer's disease mutation database (http://molgenwww.uia.ac.be/ADMutations) lead to increased generation of the highly amyloid plaque-prone Aβ42 peptide from APP.
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Details
- Title
- Welcome to the complex disease world
- Creators
- Aleister J. Saunders - Drexel UniversityRudolph E. Tanzi - Massachusetts General Hospital
- Publication Details
- Experimental neurology, v 184(1), pp 50-53
- Publisher
- Elsevier
- Number of pages
- 4
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biology
- Web of Science ID
- WOS:000186804800011
- Scopus ID
- 2-s2.0-0344826517
- Other Identifier
- 991021448157104721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences