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Cited by 128Alzheimer's disease research and treatmentsNerve injury and regenerationNeuroscience and Neuropharmacology Research

Impaired neuronal plasticity in transgenic mice expressing human apolipoprotein E4 compared to E3 in a model of entorhinal cortex lesion.

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White, F., Nicoll, J.A.R., Roses, A.D., Horsburgh, K.·2001·Neurobiology of Disease
DOI 10.1006/nbdi.2001.0401
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Abstract

The apolipoprotein E (APOE) epsilon 4 allele is a major risk factor for late-onset familial and sporadic Alzheimer's disease (AD) and is associated with a poor outcome after brain injury. Each apoE isoform is suggested to have differential effects on neuronal repair mechanisms within the CNS. In the present study, APOE genotype influence on the immediate response to injury and subsequent repair process was examined in a line of transgenic APOE mice possessing human APOE gene insertions (epsilon 3 and epsilon 4). Quantification of synaptophysin and GAP-43 immunoreactivity was used to measure the extent of degeneration and regeneration after entorhinal cortex lesion (ECL). Progressive neurodegenerative decline occurred in the ipsilateral dentate gyrus until day 28 post-ECL which was more severe in APOE epsilon 3 mice compared to APOE epsilon 4 mice. By day 90 post-ECL compensatory sprouting and reactive synaptogenesis had taken place in the dentate gyrus of APOE epsilon 3 mice such that GAP-43 and synaptophysin immunoreactivity had returned to prelesion levels. In contrast, APOE epsilon 4 mice displayed significant deficits in synaptophysin and GAP-43 immunostaining compared to the APOE epsilon 3 mice (P < 0.05). Expansion of the inner molecular layer (IML) was used as a measure of the sprouting index from the commissural-associational pathway and by day 90 post-ECL the IML width in APOE epsilon 3 mice had increased by 45% but only 20% in APOE epsilon 4 mice (P < 0.0001). ApoE…

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  • Compensatory sprouting after entorhinal cortex lesion was impaired in transgenic mice expressing apoE4 under the control of human promoter, compared with apoE3 transgenic mice.

    “compensatory sprouting after entorhinal cortex lesion was impaired in transgenic mice expressing apoE4 under the control of human promoter, compared with apoE3 transgenic mice (White et al., 2001).”

    From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as White et al., 2001

  • Compared with apoE3 transgenic mice, apoE4 transgenic mice had impaired compensatory sprouting and synaptogenesis after entorhinal cortex lesion.

    “Compared with apoE3 transgenic mice, apoE4 transgenic mice had impaired compensatory sprouting and synaptogenesis after entorhinal cortex lesion (White et al., 2001)”

    From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as White et al., 2001

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Authors
White, F., Nicoll, J. A. R., Roses, A. D., & Horsburgh, K.
Affiliations
University of Glasgow (GB)
ORCID
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2001-08
Volume
8
Issue
4
Pages
611-625
ISSN
0969-9961 (ISSN-L)
DOI
10.1006/nbdi.2001.0401
OpenAlex
W2063723612
Cited by
128
References
65
Citations by year
2025: 2 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 7 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 7 · 2016: 7 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 2
FWCI
5.89
Type
journal article
Language
en
Open access
Licence
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • ePrints Soton (University of Southampton) (submittedVersion)
Funders
  • Institute of Museum and Library Services
  • University of Glasgow
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
apolipoprotein E, APOE ε4, neuroplasticity, entorhinal cortex lesion, dentate gyrus, synaptogenesis, axonal sprouting, GAP-43, synaptophysin, neurodegeneration, Alzheimer's disease risk, transgenic mice, brain injury recovery
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Disease Models, Animal, Genotype, Humans, Mice, Inbred C57BL, Mice, Transgenic, Nerve Degeneration, Neuronal Plasticity, Gene Expression, Entorhinal Cortex, Mice, Apolipoprotein E3, Apolipoprotein E4

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