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Cited by 39Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

ApoE mimetic improves pathology and memory in a model of Alzheimer’s disease

Krishnamurthy, Kamesh, Cantillana, Viviana, Wang, Haichen, Sullivan, Patrick M., Kolls, Bradley J., Ge, Xintong, Lin, Yufeng, Mace, Brian +1 more·2020·Brain Research
DOI 10.1016/j.brainres.2020.146685
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Abstract

Alzheimer's disease (AD) is the most common form of dementia and is characterized pathologically by Aβ plaques. Current treatments are purely symptomatic despite decades of intensive research interest. Notably, patients with the APOE4 allele are at increased risk for developing AD. One hypothesis regarding the mechanism by which the APOE4 allele might increase AD risk is loss of adaptive function, raising the possibility that the exogenous administration of apoE mimetics would have therapeutic effects. In this study, we utilized a previously characterized murine model of AD containing human APP, PS1 and APOE4TR, the APP/PS1/APOETR mouse. We treated male APP/PS1/APOETR mice with the apoE mimetic CN-105 or vehicle for 40d, beginning either at 14-18 or 25-28 weeks of age. After termination of treatment we tested animals in both Morris water maze and contextual fear conditioning, and examined soluble Aβ by biochemistery and Aβ deposition in cortex by unbiased stereology. We found that transient treatment with CN-105 for 40d beginning at 14-18 weeks reduced Aβ pathology and rescued memory deficits in male APP/PS1/APOETR mice. Notably, delaying treatment onset to 25-28 weeks did not produce as robust an effect. These results suggest CN-105 treatment in a mouse model of AD results in a reduction in AD pathology and improved behavioral outcomes when administered early in the course of disease. As CN-105 has an excellent safety profile and is already in clinical trials, these findings…

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  • APOE mimetics (small peptides homologous to the receptor-binding region of APOE) have been shown to prevent microglial reaction in vitro, as well as Aβ deposition and associated memory deficits in APOE4 plaque-depositing mice.

    “Such APOE mimetics have been shown to prevent microglial reaction in vitro, as well as Aβ deposition and associated memory deficits in APOE4 plaque-depositing mice195,196.”

    From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [196]

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Authors
Krishnamurthy, K., Cantillana, V., Wang, H., Sullivan, P. M., Kolls, B. J., Ge, X., Lin, Y., Mace, B., & Laskowitz, D. T.
Affiliations
  • Duke University (US)
  • Tianjin Medical University General Hospital (CN)
Corresponding author
Krishnamurthy, Kamesh
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2020-04
Volume
1733
Pages
146685
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2020.146685
OpenAlex
W3003733049
Cited by
39
References
12
Citations by year
2026: 3 · 2025: 9 · 2024: 5 · 2023: 4 · 2022: 10 · 2021: 6 · 2020: 2
FWCI
3.31
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (T32-GM007171)
  • American Epilepsy Society
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
Alzheimer's disease, APOE ε4, amyloid plaques, memory impairment, treatment timing, early intervention, soluble amyloid-beta, contextual fear conditioning, Morris water maze
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Behavior, Animal, Brain, Disease Models, Animal, Male, Memory, Mice, Transgenic, Amyloid beta-Peptides, Protein Aggregation, Pathological

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