Amyloid β and free heme: bloody new insights into the pathogenesis of Alzheimer's disease
J(o)rg Flemmig
Marcel Zámock(y)
A Alia
摘要：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.
机标关键词：
资助基金：The work was supported by the Alzheimer Forschung Initiative e.V.(AFI 13810)
论文发表日期：2018-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：5( 1170-1174 )
英文信息