Amyloid-β: the seeds of darkness.

Abstract

Whilst the amyloid-β (Aβ) hypothesis/centric theory continues to evolve, genetic, biochemical and pathological evidence still suggests that Aβ is central to the etiology of Alzheimer's disease (AD). In particular, Aβ-oligomers/soluble Aβ, may be an earlier determinant of Alzheimer's disease and better correlative of cognitive impairment. Whilst there are a number of Aβ-oligomeric species in existence (making therapeutic and diagnostic biomarker choice cumbersome), their existence is in equilibrium with Aβ-fibrils, the main constituent of cored plaques. Although Alzheimer's disease remains incurable, improvements to Aβ immunotherapies and strategies to target Aβ continue to evolve, with the reliance upon Aβ imaging to shed light on the outcome of therapeutics proving very useful.

• Authors: Michelle T Fodero-Tavoletti, Victor L Villemagne, Christopher C Rowe, Colin L Masters, Kevin J Barnham, Roberto Cappai
• Journal: The international journal of biochemistry & cell biology (Int J Biochem Cell Biol) Vol. 43 Issue 9 Pg. 1247-51 (Sep 2011) ISSN: 1878-5875 [Electronic] Netherlands
• PMID: 21601003 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2011 Elsevier Ltd. All rights reserved.

Chemical References

• Amyloid beta-Peptides
• Protein Isoforms

Topics

• Alzheimer Disease (etiology, metabolism, pathology)
• Amino Acid Sequence
• Amyloid beta-Peptides (chemistry, genetics, metabolism)
• Animals
• Clinical Trials as Topic
• Gene Expression
• Humans
• Molecular Sequence Data
• Protein Conformation
• Protein Isoforms