Blocking the apolipoprotein E/Amyloid β interaction in triple transgenic mice ameliorates Alzheimer's disease related amyloid β and tau pathology

• DOI: 10.1111/jnc.12484
• Publication Date: 2013-10-12T02:32:18Z
• Authors: Shan Liu; Ariel Breitbart; Yanjie Sun; Pankaj D. Mehta; Allal Boutajangout; Henrieta Scholtzova; Thomas Wisniewski
• Keywords: Apolipoprotein E; Amyloid (mycology)

Inheritance of the apolipoprotein E4 (apoE4) genotype has been identified as major genetic risk factor for late-onset Alzheimer's disease (AD). Studies have shown that binding between apoE and amyloid-β (Aβ) peptides occurs at residues 244-272 12-28 Aβ. ApoE4 implicated in promoting Aβ deposition impairing clearance We hypothesized blocking apoE/Aβ interaction would serve an effective new approach to AD therapy. previously treatment with Aβ12-28P can reduce amyloid plaques APP/PS1 transgenic (Tg) mice vascular TgSwDI congophilic angiopathy. In present study, we investigated whether elicits a therapeutic effect on tau-related pathology addition using old triple (3xTg, PS1M146V , APPSwe tauP30IL transgenes) established from ages 21 26 months. show substantially reduces tau both immunohistochemically biochemically, well reducing burden suppressing activation astrocytes microglia. These affects correlate behavioral amelioration treated Tg mice.