Affiliations: [a] Department of Pathology, The University of Melbourne, Parkville, Melbourne, VIC, Australia | [b] Neuroproteomics Platform, Bio21 Molecular Science and Biotechnology Institute, VIC, Australia | [c] Mental Health Research Institute, The University of Melbourne, Parkville, Melbourne, VIC, Australia | [d] Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, VIC, Australia | [e] Department of Pharmacology, The University of Melbourne, Parkville, Melbourne, VIC, Australia
Correspondence:
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Correspondence to: Kevin J. Barnham, MHRI and Department of Pharmacology, The University of Melbourne, VIC 3010, Australia. Tel.: +61 3 83442555; Fax: +61 3 93476750; E-mail: kbarnham@unimelb.edu.au.
Abstract: Over the past 100 years, there has been an exponential increase in our understanding of the underlying pathology of Alzheimer's disease (AD). This growth in knowledge has largely stemmed from the intensification of research into AD which has occurred over the past three decades and the incorporation of the amyloid cascade hypothesis as the generally accepted dogma of AD pathogenesis. While at times contentious, the notion that AD arises from aberrations in amyloid-β (Aβ) production and degradation has led to a number of significant breakthroughs in the way in which AD is currently diagnosed and in the attempts at disease modifying therapies, from investigations into the underlying factors mediating the aggregation of Aβ to the development of therapeutic strategies and measures of neuroimaging allowing Aβ burden to be monitored within the AD-affected brain. This review focuses on some of the recent work we have conducted toward elucidating the role of Aβ in AD.
Keywords: Biomarker, blood, copper, mass spectrometry, metal chaperone, NMDA, toxicity, zinc
