Neurodegeneration and cognitive impairment in apoE-deficient mice is ameliorated by infusion of recombinant apoE.
Abstract
Recent studies suggest that apolipoprotein E (apoE) might play a neurotrophic function in the central nervous system and that altered functioning of this molecule could result in neurodegeneration. The main objective of this study was to determine if neurodegenerative and cognitive alterations in apoE-deficient mice are reversible by infusion of recombinant apoE into the lateral ventricles. ApoE-deficient mice treated with either apoE3 or apoE4 showed a significant improvement in their learning capacity in the Morris water maze compared to saline-infused apoE-deficient mice. While this improved performance was associated with restoration of neuronal structure, the poor learning ability of apoE-deficient mice treated with saline correlated with the disrupted synapto-dendritic structure. This study supports the contention that apoE might play a neurotrophic effect in vivo and suggests that apoE might have a potential therapeutic role.
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Both negative effects and minor beneficial effects on neurites and synaptic functions have been associated with apoE4.
“Both negative effects and minor beneficial effects on neurites and synaptic functions have been associated with apoE4 (Cambon et al., 2000; Masliah et al., 1997; Veinbergs et al., 1999).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Masliah et al., 1997
The effects of apoE4 on synaptic plasticity were inconsistent among studies.
“the effects of apoE4 on synaptic plasticity were inconsistent among studies.”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Masliah et al., 1997
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The role of apolipoprotein E in Alzheimer's disease
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“Both negative effects and minor beneficial effects on neurites and synaptic functions have been associated with apoE4 (Cambon et al., 2000; Masliah et al., 1997; Veinbergs et al., 1999).”
BackgroundLitvinchuk, A., Huynh, T. V., Shi, Y., Jackson, R. J., Finn, M. B., Manis, M., Francis, C. M., Tran, A. C., Sullivan, P. M., Ulrich, J. D., et al. (2021) · Annals of Neurology · doi:10.1002/ana.26043 · Cited by 91 · see citing works
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Opposing Roles of apolipoprotein E in aging and neurodegeneration
Hudry, E., Klickstein, J., Cannavo, C., Jackson, R., Muzikansky, A., Gandhi, S., Urick, D., Sargent, T., Wrobleski, L., Roe, A. D., et al. (2019) · Life Science Alliance · doi:10.26508/lsa.201900325 · Cited by 30 · see citing works
- Authors
- Masliah, E., Samuel, W., Veinbergs, I., Mallory, M., Mante, M., & Saitoh, T.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Masliah, Eliezer
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 1997-03
- Volume
- 751
- Issue
- 2
- Pages
- 307-314
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1979395651
- Cited by
- 146
- References
- 1
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 5 · 2014: 2 · 2013: 4 · 2012: 5
- FWCI
- 8.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli and Edythe Broad Foundation
- Ruth K. Broad Biomedical Research Foundation
- National Institutes of Health
- National Institute on Aging (AG10689, AG05131, R01AG010689, P50AG005131)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- apolipoprotein E, ApoE-deficient mice, neurodegeneration, cognitive impairment, lateral ventricle infusion, neurotrophic effects, learning and memory, Morris water maze, neuronal structure, APOE3, APOE ε4, neuroprotection
- MeSH terms
- Animals, Apolipoproteins E, Cognition, Cognition Disorders, Dendrites, Injections, Intraventricular, Isomerism, Mice, Inbred C57BL, Mice, Mutant Strains, Nerve Degeneration, Recombinant Proteins, Synapses, Mice
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