The synthesized transporter K16APoE enabled the therapeutic HAYED peptide to cross the blood-brain barrier and remove excess iron and radicals in the brain, thus easing Alzheimer's disease

Drug Deliv Transl Res. 2019 Feb;9(1):394-403. doi: 10.1007/s13346-018-0579-4.


Alzheimer's disease (AD) is currently incurable and places a large burden on the caregivers of AD patients. In the AD brain, iron is abundant, catalyzing free radicals and impairing neurons. The blood-brain barrier hampers antidementia drug delivery via circulation to the brain, which limits the therapeutic effects of drugs. Here, according to the method described by Gobinda, we synthesized a 16 lysine (K) residue-linked low-density lipoprotein receptor-related protein (LRP)-binding amino acid segment of apolipoprotein E (K16APoE). By mixing this protein with our designed therapeutic peptide HAYED, we successfully transported HAYED into an AD model mouse brain, and the peptide scavenged excess iron and radicals and decreased the necrosis of neurons, thus easing AD.

Keywords: Alzheimer’s disease; Blood-brain barrier; HAYED peptide; Iron; K16APoE; Radical.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Animals
  • Apolipoproteins E / chemistry*
  • Apolipoproteins E / metabolism
  • Biological Transport
  • Blood-Brain Barrier / drug effects
  • Disease Models, Animal
  • Humans
  • Iron / chemistry
  • Low Density Lipoprotein Receptor-Related Protein-1 / chemistry*
  • Mice
  • Peptides / administration & dosage*
  • Peptides / chemistry


  • Apolipoproteins E
  • Low Density Lipoprotein Receptor-Related Protein-1
  • Peptides
  • Iron