The amyloid-β peptide (Aβ) is widely considered to be the major toxic agent in the pathogenesis of Alzheimer's disease, a condition which afflicts approximately 36 million people worldwide. Despite a plethora of studies stretching back over two decades, identifying the toxic Aβ species has proved difficult. Debate has centred on the Aβ fibril and oligomer. Despite support from numerous experimental models, important questions linger regarding the role of the Aβ oligomer in particular. It is likely a huge array of oligomers, rather than a single species, which cause toxicity. Reappraisal of the role of the Aβ fibril points towards a dynamic relationship with the Aβ oligomer within an integrated system, as supported by evidence from microglia. However, some continue to doubt the pathological role of amyloid β, instead proposing a protective role. If the field is to progress, all Aβ oligomers should be characterised, the nomenclature revised and a consistent experimental protocol defined. For this to occur, collaboration will be required between major research groups and innovative analytical tools developed. Such action must surely be taken if amyloid-based therapeutic endeavour is to progress.
- MOLECULAR PATHOLOGY
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.