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Cited by 142Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Apolipoprotein E and β-amyloid levels in the hippocampus and frontal cortex of Alzheimer's disease subjects are disease-related and apolipoprotein E genotype dependent

Beffert, Uwe, Cohn, Jeffrey S, Petit-Turcotte, Caroline, Tremblay, Michel, Aumont, Nicole, Ramassamy, Charles, Davignon, Jean, Poirier, Judes·1999·Brain Research
DOI 10.1016/s0006-8993(99)01894-6
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Abstract

The epsilon4 allele of apolipoprotein E (apoE) is associated with increased risk for the development of Alzheimer's disease (AD), possibly due to interactions with the beta-amyloid (Abeta) protein. The mechanism by which these two proteins are linked to AD is still unclear. To further assess their potential relationship with the disease, we have determined levels of apoE and Abeta isoforms from three brain regions of neuropathologically confirmed AD and non-AD tissue. In two brain regions affected by AD neuropathology, the hippocampus and frontal cortex, apoE levels were found to be decreased while Abeta(1-40) levels were increased. Levels of apoE were unchanged in AD cerebellum. Furthermore, levels of apoE and Abeta(1-40) were found to be apoE genotype dependent, with lowest levels of apoE and highest levels of Abeta(1-40) occurring in epsilon4 allele carriers. These results suggest that reduction in apoE levels may give rise to increased deposition of amyloid peptides in AD brain.

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Crossref · 10.1016/s0006-8993(99)01894-6

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  • The effect of the ε4 allele on locally synthesized CNS apoE protein levels is less clear, with conflicting reports showing reduced levels, no change, or increases in apoE from AD patient CNS and animal models.

    “The effect of the ␧4 allele on the locally synthesized CNS apoE protein levels is less clear with multiple conflicting reports showing either reduced levels (Bertrand et al., 1995;Beffert et al., 1999;Glo ¨ckner et al., 2002;Poirier, 2005;Ramaswamy et al., 2005), no change (Sullivan et al., 2004;Fryer et al., 2005) or increases (Fukumoto et al., 2003) in apoE from both AD patient CNS and animal mo”

    From Impact of Apolipoprotein E (ApoE) Polymorphism on Brain ApoE Levels (2008) · cites this paper as Beffert et al., 1999

  • ApoE4 carriers have increased Aβ burden.

    “apoE4 carriers have increased A␤ burden (Beffert et al., 1999;Corder et al., 2004;Fryer et al., 2005).”

    From Impact of Apolipoprotein E (ApoE) Polymorphism on Brain ApoE Levels (2008) · cites this paper as Beffert et al., 1999

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Authors
Beffert, U., Cohn, J. S., Petit-Turcotte, C., Tremblay, M., Aumont, N., Ramassamy, C., Davignon, J., & Poirier, J.
Affiliations
  • Douglas Mental Health University Institute (CA)
  • Montreal Clinical Research Institute (CA)
Corresponding author
Poirier, Judes
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
1999-10
Volume
843
Issue
1-2
Pages
87-94
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/s0006-8993(99)01894-6
OpenAlex
W2068216402
Cited by
142
References
5
Citations by year
2026: 1 · 2025: 2 · 2024: 9 · 2023: 4 · 2022: 5 · 2021: 6 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 1 · 2014: 9 · 2013: 7 · 2012: 7
FWCI
3.17
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
apolipoprotein E, amyloid-beta, Alzheimer's disease, APOE ε4, hippocampus, frontal cortex, amyloid deposition, APOE genotype, Aβ40, cerebellum
MeSH terms
Aged, Alzheimer Disease, Apolipoproteins E, Cerebellum, Female, Frontal Lobe, Genotype, Hippocampus, Humans, Male, Reference Values, Amyloid beta-Peptides

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