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Cited by 104Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchAlzheimer's disease research and treatments

Susceptibility of transgenic mice expressing human apolipoprotein E to closed head injury: The allele E3 is neuroprotective whereas E4 increases fatalities

Sabo, T, Lomnitski, L, Nyska, A, Beni, S, Maronpot, R.R, Shohami, E, Roses, A.D, Michaelson, D.M·2000·Neuroscience
DOI 10.1016/s0306-4522(00)00438-3
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Abstract

Apolipoprotein E, the major brain lipid-binding protein, is expressed in humans as three common isoforms (E2, E3 and E4). Previous studies revealed that the allele apolipoprotein E4 is a major genetic risk factor of Alzheimer's disease and that traumatic brain injury is associated with increased risk for developing this disease. Furthermore, it has been suggested that the effects of traumatic head injury and apolipoprotein E4 in Alzheimer's disease are synergistic. To test the hypothesis that the apolipoprotein E genotype affects susceptibility to brain injury, we subjected transgenic mice, expressing either human apolipoprotein E3 or human apolipoprotein E4 on a null mouse apolipoprotein E background and apolipoprotein E-deficient knockouts, to closed head injury and compared mortality, neurological recovery and the extent of brain damage of the survivors. More than 50% of the transgenic mice expressing human apolipoprotein E4 died following closed head injury, whereas only half as many of the transgenic mice expressing human apolipoprotein E3, and of the control and apolipoprotein E-deficient mice died during this period (P<0.02). A neurological severity score used for clinical assessment of the surviving mice up to 11 days after closed head injury revealed that the four mouse groups displayed similar severity of damage at 1h following injury. At three and 11 days post-injury, however, the neurological severity scores of the transgenic mice expressing human apolipoprotein E…

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Crossref · 10.1016/s0306-4522(00)00438-3

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  • ApoE knock-out mice and ε4/4 targeted replacement mice exhibit more severe neurological and cognitive deficits after closed head injury, experimental stroke, entorhinal cortex lesions, and experimental allergic encephalomyelitis than controls.

    “apoE knock-out mice and ␧4/4 targeted replacement mice exhibit more severe neurological and cognitive deficits after closed head injury (Chen et al., 1997;Sabo et al., 2000), experimental stroke (Laskowitz et al., 1997;Sheng et al., 1998Sheng et al., , 1999)), entorhinal cortex lesions (Fagan et al., 1998;White et al., 2001) and experimental allergic encephalomyelitis (Karussis et al., 2003) than”

    From Impact of Apolipoprotein E (ApoE) Polymorphism on Brain ApoE Levels (2008) · cites this paper as Sabo et al., 2000

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Authors
Sabo, T., Lomnitski, L., Nyska, A., Beni, S., Maronpot, R. R., Shohami, E., Roses, A. D., & Michaelson, D. M.
Affiliations
  • Tel Aviv University (IL)
  • National Institute of Environmental Health Sciences (US)
  • Hebrew University of Jerusalem (IL)
Corresponding author
Michaelson, D.M
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2000-11
Volume
101
Issue
4
Pages
879-884
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/s0306-4522(00)00438-3
OpenAlex
W1973633053
Cited by
104
References
7
Citations by year
2022: 3 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 3
FWCI
6.11
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
apolipoprotein E, APOE ε4, apolipoprotein E3, closed head injury, traumatic brain injury, neuroprotection, transgenic mice, mortality, neurological recovery, brain damage, Alzheimer's disease risk
MeSH terms
Alleles, Animals, Apolipoproteins E, Brain, Humans, Mice, Inbred C57BL, Mice, Transgenic, Nervous System, Reference Values, Head Injuries, Closed, Neuroprotective Agents, Genetic Predisposition to Disease, Mice, Apolipoprotein E4

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