Differential neurotrophic effects of apolipoprotein E in aged transgenic mice.
Abstract
The present study seeked to determine whether the neurodegenerative and cognitive alterations in aged apolipoprotein E-deficient mice are differentially reversed by transgenic overexpression of human apolipoprotein-E3 vs. apolipoprotein-E4 in the background of deficient endogenous apolipoprotein E. These studies showed dendritic alterations in pyramidal neurons of apolipoprotein-E4 transgenic mice, similar to the ones observed in apolipoprotein E-deficient mice. However, these mice had a preserved density of synaptophysin-immunoreactive presynaptic terminals. In contrast, mice overexpressing apolipoprotein-E3 showed no synapto-dendritic alterations. Analysis of behavioral performance in the Morris water maze showed that while apolipoprotein E-deficient mice performed poorly, overexpression of apolipoprotein-E3 and, to a lower extent apolipoprotein-E4, resulted in an improved performance. This study supports the contention that, compared with apolipoprotein-E4, apolipoprotein-E3 might have a greater neurotrophic in vivo effect in aged mice.
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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 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 Veinbergs et al., 1999
Cites
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Self-citationJi, Z.-S., Pitas, R. E., & Mahley, R. W. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.22.13452 · Cited by 134 · see citing works
Fagan, A. M., Murphy, B. A., Patel, S. N., Kilbridge, J. F., Mobley, W. C., Bu, G., & Holtzman, D. M. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6818 · Cited by 116 · see citing works
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The role of apolipoprotein E in Alzheimer's disease
Kim, J., Basak, J. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.06.026 · Cited by 1,661 · see citing works
Apolipoprotein E and cholesterol in aging and disease in the brain
de Chaves, E. P., Narayanaswami, V., Christoffersen, C., & Nielsen, L. B. (2008) · Future Lipidology · doi:10.2217/17460875.3.5.505 · Cited by 164 · see citing works
Tzioras, M., Davies, C., Newman, A., Jackson, R., & Spires‐Jones, T. (2019) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12529 · Cited by 147 · see citing works
Kim, J., Yoon, H., Basak, J., & Kim, J. (2014) · Molecules and Cells · doi:10.14348/molcells.2014.0248 · Cited by 141 · see citing works
“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).”
BackgroundInfluentialHippocampus-related cognitive impairments in young apoE4 targeted replacement mice
Salomon-Zimri, S., Boehm-Cagan, A., Liraz, O., & Michaelson, D. M. (2013) · Neurodegenerative Diseases · doi:10.1159/000354777 · Cited by 34 · see citing works
- Authors
- Veinbergs, I., Mallory, M., Mante, M., Rockenstein, E., Gilbert, J. R., & Masliah, E.
- Affiliations
- University of California San Diego (US)
- Duke University (US)
- Corresponding author
- Masliah, Eliezer
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1999-04
- Volume
- 265
- Issue
- 3
- Pages
- 218-222
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2015420496
- Cited by
- 46
- References
- 3
- Citations by year
- 2022: 2 · 2018: 2 · 2015: 1 · 2014: 3 · 2013: 6 · 2012: 1
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r29ag010869-05)
- National Institute on Aging (AG10869)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- apolipoprotein E, apolipoprotein E3, APOE ε4, neurotrophic effects, aging, transgenic overexpression, ApoE-deficient mice, pyramidal neurons, synaptophysin, presynaptic terminals, cognitive impairment, spatial learning, neurodegeneration
- MeSH terms
- Aging, Alzheimer Disease, Animals, Apolipoproteins E, Brain Chemistry, Cognition, Dendrites, Frontal Lobe, Humans, Microtubule-Associated Proteins, Nerve Degeneration, Synapses, Mice, Knockout, Microscopy, Confocal, Maze Learning, GAP-43 Protein, Mice, Apolipoprotein E3, Apolipoprotein E4
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