The Abeta hypothesis: leading us to rationally-designed therapeutic strategies for the treatment or prevention of Alzheimer disease

Brain Pathol. 2005 Jan;15(1):84-7. doi: 10.1111/j.1750-3639.2005.tb00104.x.

Abstract

In recent years the amyloid cascade hypothesis of Alzheimer disease (AD) has been increasingly referred to as the amyloid beta protein (Abeta) cascade hypothesis. This subtle rephrasing reflects the acknowledgment that there is debate within the field as to whether Abeta aggregates other than Abeta deposited as classic amyloid fibrils could trigger the pathological cascade that results in neuronal dysfunction and neurodegeneration. Despite this semantic shift, which highlights one enigmatic aspects of AD, the evidence supporting the Abeta hypothesis of AD is extensive. More importantly the Abeta hypothesis of AD has led and will continue to lead to the development of rationale therapeutic strategies that are likely to either prevent or treat this devastating disease. In this review, the evidence supporting the Abeta hypothesis and the recent advances in anti-Abeta therapy are discussed.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology*
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Brain / pathology*
  • Humans
  • Models, Neurological*

Substances

  • Amyloid beta-Peptides