Physiologic and Neurotoxic Properties of Aβ Peptides

  • Gillian C. Gregory
  • Claire E. Shepherd
  • Glenda M. Halliday


Alzheimer’s disease (AD) is characterized by a gradual decline of numerous cognitive processes, culminating in dementia and neurodegeneration. It is the most common form of dementia and a significant cause of death in the elderly. Definitive diagnosis of AD requires the presence of the extracellular accumulation of Aβ peptides in senile plaques in the cortex of the brain (Fig. 11.1) [1]. β-Amyloid (Aβ) peptides are ∼4-kDa polypeptides with the main alloforms consisting of 40 and 42 amino acids. Analysis of the insoluble protein fraction has identified the longer Aβ42 alloform as the predominant peptide species in the neuropathologic accumulations (see [2]), although Aβ peptides of variable length accumulate within plaques [3]–[8]. The association between the abnormal accumulation of Aβ peptides in the brain and dementia is strong evidence that Aβ peptides are vital for normal brain functioning.


Amyloid Precursor Protein Amyloid Beta Neurobiol Aging Amyloid Beta Protein Neurotoxic Property 
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Copyright information

© Springer-Verlag London Limited 2007

Authors and Affiliations

  • Gillian C. Gregory
    • 1
  • Claire E. Shepherd
    • 1
  • Glenda M. Halliday
    • 2
  1. 1.Prince of Wales Medical Research InstituteUniversity of New South WalesSydneyAustralia
  2. 2.University of New South WalesPrince of Wales Medical Research InstituteRanwick SydneyAustralia

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