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Brain Advance Access originally published online on September 29, 2006
Brain 2006 129(11):2823-2839; doi:10.1093/brain/awl251
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Review Articles

Alzheimer's centennial legacy: prospects for rational therapeutic intervention targeting the Aß amyloid pathway

Colin L. Masters1 and Konrad Beyreuther2

1 Department of Pathology, The University of Melbourne and the Mental Health Research Institute of Victoria Parkville, Victoria, Australia 2 Centre for Molecular Biology, The University of Heidelberg Heidelberg, Germany

Correspondence to: Colin L. Masters, Department of Pathology, The University of Melbourne, 3010, Victoria, Australia E-mail: c.masters{at}unimelb.edu.au

It is now 100 years since the nosological definition of Alzheimer's disease emerged. In the first 80 years, very little progress was made in understanding the mechanisms that caused the brain to degenerate in a remarkably specific fashion (amyloid accumulation with neurofibrillary changes). Over the past 20 years, there has been an explosion of knowledge which continues today at an exponential rate. The molecular pathways underlying the synaptic dysfunction in Alzheimer's disease have delivered many validated therapeutic and diagnostic targets. A variety of therapeutic strategies aimed at disease modification are now in clinical development.

Key Words: Aß amyloid pathway; Alzheimer's disease; amyloid beta precursor protein

Abbreviations: Aß, amyloid ß peptide; AChE, acetylcholinesterase; AChE-I, AChE inhibitors; APP, amyloid beta (A4) precursor protein; MPAC, metal–protein attenuating compounds; NMDA, N-methyl-D-aspartate

Received July 3, 2006. Revised August 15, 2006. Accepted August 16, 2006.


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