Key factors in Alzheimer's disease: β-Amyloid precursor protein processing, metabolism and intraneuronal transport

Thomas A. Bayer, Oliver Wirths, Katalin Majtényi, Tobias Hartmann, Gerd Multhaup, Konrad Beyreuther, Christian Czech

Research output: Contribution to journalReview article

153 Citations (Scopus)

Abstract

During the last years it has become evident that the β-amyloid (Aβ) component of senile plaques may be the key molecule in the pathology of Alzheimer's disease (AD). The source and place of the neurotoxic action of Aβ, however, is still a matter of controversy. The precursor of the β-amyloid peptide is the predominantly neuronal β-amyloid precursor protein. We, and others, hypothesize that intraneuronal misregulation of APP leads to an accumulation of Aβ peptides in intracellular compartments. This accumulation impairs APP trafficking, which starts a cascade of pathological changes and causes the pyramidal neurons to degenerate. Enhanced Aβ secretion as a function of stressed neurons and remnants of degenerated neurons provide seeds for extracellular Aβ aggregates, which induce secondary degenerative events involving neighboring cells such as neurons, astroglia and macrophages/microglia.

Original languageEnglish
Pages (from-to)1-11
Number of pages11
JournalBrain Pathology
Volume11
Issue number1
Publication statusPublished - Jan 1 2001

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ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)
  • Clinical Neurology

Cite this

Bayer, T. A., Wirths, O., Majtényi, K., Hartmann, T., Multhaup, G., Beyreuther, K., & Czech, C. (2001). Key factors in Alzheimer's disease: β-Amyloid precursor protein processing, metabolism and intraneuronal transport. Brain Pathology, 11(1), 1-11.