Blocking the apolipoprotein E/Amyloid β interaction in triple transgenic mice ameliorates Alzheimer's disease related amyloid β and tau pathology
Open accessAbstract
Inheritance of the apolipoprotein E4 (apoE4) genotype has been identified as the major genetic risk factor for late‐onset Alzheimer's disease (AD). Studies have shown that the binding between apoE and amyloid‐β (Aβ) peptides occurs at residues 244–272 of apoE and residues 12–28 of Aβ. ApoE4 has been implicated in promoting Aβ deposition and impairing clearance of Aβ. We hypothesized that blocking the apoE/Aβ interaction would serve as an effective new approach to AD therapy. We have previously shown that treatment with Aβ12‐28P can reduce amyloid plaques in APP/PS1 transgenic (Tg) mice and vascular amyloid in TgSwDI mice with congophilic amyloid angiopathy. In the present study, we investigated whether the Aβ12‐28P elicits a therapeutic effect on tau‐related pathology in addition to amyloid pathology using old triple transgenic AD mice (3xTg, with PS1 M146V, APP Swe and tau P30IL transgenes) with established pathology from the ages of 21 to 26 months. We show that treatment with Aβ12‐28P substantially reduces tau pathology both immunohistochemically and biochemically, as well as reducing the amyloid burden and suppressing the activation of astrocytes and microglia. These affects correlate with a behavioral amelioration in the treated Tg mice. image The apolipoprotein E (apoE)/amyloid beta (Aβ) interaction plays an important role in the aggregation and clearance of Aβ. We show that the apoE/Aβ binding blocker, Aβ12‐28P, elicits a therapeutic effect on tau related pathology, in addition to amyloid deposition, in 3xTg Alzheimer's disease model mice. These affects correlate with a behavioral amelioration in the treated Tg mice. We believe this presents a novel therapeutic approach for AD.
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A small molecule mimetic homologous to the domain of Aβ that interacts with APOE but modified to be more protease-resistant can reduce the oligomerization of Aβ in vitro and ameliorate Aβ and tau pathology in a triple transgenic mouse model of AD.
“this has been achieved using a small molecule mimetic homologous to the domain of Aβ that interacts with APOE but is modified to be more protease-resistant. This small peptide can reduce the oligomerization of Aβ in vitro and ameliorate Aβ and tau pathology in a triple transgenic mouse model of AD193,194”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [194]
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Experimental — accuracy not yet measuredIn mouse models, blocking the apoE:Aβ interaction can have significant effects on amyloid and tangle formation.
“And in mouse models blocking the apoE:Aβ interaction can have significant effects on amyloid and tangle formation [16].”
From Discovery of a Missense Mutation (Q222K) of the <i>APOE</i> Gene from the Australian Imaging, Biomarker and Lifestyle Study (2023) · cites this paper as [16]
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Cites
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BackgroundSelf-citationHuman ApoE isoforms differentially regulate brain amyloid-β peptide clearance
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- Authors
- Liu, S., Breitbart, A., Sun, Y., Mehta, P. D., Boutajangout, A., Scholtzova, H., & Wisniewski, T.
- Affiliations
- New York University (US)
- Department of Immunology New York State Institute for Basic Research in Developmental Disabilities Staten Island NY USA
- King Abdulaziz University (SA)
- Departments of Neurology Pathology and Psychiatry New York University School of Medicine ERSP New York NY USA
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2013-11-06
- Volume
- 128
- Issue
- 4
- Pages
- 577-591
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC3946231
- OpenAlex
- W2042058045
- Cited by
- 60
- References
- 15
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 5 · 2023: 6 · 2022: 4 · 2021: 4 · 2020: 4 · 2019: 7 · 2018: 5 · 2017: 4 · 2016: 3 · 2015: 5 · 2014: 2 · 2013: 1
- FWCI
- 2.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (AG20245, NS073502)
- Alzheimer's Drug Discovery Foundation
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, amyloid-beta, Alzheimer's disease, tau pathology, triple transgenic mice, amyloid plaques, astrocyte activation, microglial activation, cognitive behavior, APOE ε4, therapeutic target
- MeSH terms
- Alzheimer Disease, Amino Acid Sequence, Amyloidosis, Animals, Apolipoproteins E, Brain Chemistry, Enzyme-Linked Immunosorbent Assay, Postural Balance, Exploratory Behavior, Gliosis, Immunohistochemistry, Mice, Transgenic, Molecular Sequence Data, Motor Activity, Peptide Fragments, Blotting, Western, Amyloid beta-Peptides, tau Proteins, Maze Learning, Mice
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