ORC ID , Marcel Zámocký2, A Alia3">
  • Users Online: 1941
  • Home
  • Print this page
  • Email this page
Year : 2018  |  Volume : 13  |  Issue : 7  |  Page : 1170-1174

Amyloid β and free heme: bloody new insights into the pathogenesis of Alzheimer’s disease

1 Institute for Medical Physics and Biophysics, Medical Faculty, Leipzig University, Leipzig, Germany
2 Institute of Molecular Biology, Slovak Academy of Sciences, Bratislava, Slovakia; Institute of Chemical, Environmental and Biological Engineering, Faculty of Technical Chemistry, Vienna University of Technology, Vienna, Austria
3 Institute for Medical Physics and Biophysics, Medical Faculty, Leipzig University, Leipzig, Germany; Leiden Institute of Chemistry, Faculty of Science, Leiden University, Leiden, The Netherlands

Correspondence Address:
Jörg Flemmig
Institute for Medical Physics and Biophysics, Medical Faculty, Leipzig University, Leipzig
Login to access the Email id

Source of Support: The work was supported by the Alzheimer Forschung Initiative e.V. (AFI 13810), Conflict of Interest: None

DOI: 10.4103/1673-5374.235021

Rights and Permissions

The cerebral formation of Amyloid β (Aβ) is a critical pathological feature of Alzheimer’s disease (AD). An accumulation of this peptide as senile plaques (SP) was already reported by Alois Alzheimer, the discoverer of the disease. Yet the exact contribution of Aβ to AD development remains elusive. Moreover, while extensive cerebral Aβ formation leads to fibril formation in many species, AD-like symptoms apparently depend on the highly conserved N-terminal residues R5, Y10 and H13. The amino acids were also shown to lead to the formation of Aβ-heme complexes, which exhibit peroxidase activity in the presence of H2O2. Taking together these observations we propose that the formation and enzymatic activity of the named complexes may represent an essential aspect of AD pathology. Furthermore, Aβ is also known to lead to cerebral micro-vessel destruction (CAA) as well as to hemolytic events. Thus we suggest that the Aβ-derived cerebral accumulation of blood-derived free heme represents a likely precondition for the subsequent formation of Aβ-heme complexes.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded404    
    Comments [Add]    
    Cited by others 15    

Recommend this journal