Cited by 146Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

Neurodegeneration and cognitive impairment in apoE-deficient mice is ameliorated by infusion of recombinant apoE.

Masliah, Eliezer, Samuel, William, Veinbergs, Isaac, Mallory, Margaret, Mante, Michael, Saitoh, Tsunao·1997·Brain Research

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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Crossref · 10.1016/s0006-8993(96)01420-5

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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).”
  • 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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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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