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Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions
Abstract
An increased prevalence of apolipoprotein E (ApoE) epsilon 4 allele exists in late onset familial Alzheimer's disease. We found, in sporadic Alzheimer's disease, that 62% of patients possessed an ApoE-epsilon 4 allele, compared with 20% of controls. ApoE-epsilon 4/4 patients had more senile plaques (SPs) than epsilon 3/3 patients. ApoE immunoreactivity of SPs was equivalent in both groups. Two receptors bind ApoE complexes, the low density lipoprotein (LDL) receptor and the LDL receptor-related protein (LRP). In normal brain, anti-LRP antibodies strongly stained neurons and lightly stained astrocytes; anti-LDL receptor antibodies stained only the neuropil and astrocytes. In Alzheimer's disease, SPs and reactive astrocytes were also strongly LRP immunoreactive. Colocalization of ApoE and LRP to SPs implies that these molecules may be involved in metabolism of components of SPs.
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In the citing paper
“APOE4 is the strongest genetic determinant of late-onset AD, increasing risk in a gene dose-dependent manner, whereas APOE2 confers substantial protection 1 -5 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [2]
In the citing paper
“As APOE4 carriers make up 55–75% of AD cases17–20”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [19]
In the citing paper
“Studies indicate that APOE binding is integral to some of these processes [16–20] with differences in APOE isoform-specific receptor binding affinity and lipid interactions affecting neuroinflammation, tau pathology, and amyloid plaque dynamics [21–24].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [24]
In the citing paper
“Collectively, these recent findings underscore the influence of APOE and APOE3Ch on both Aβ and tau pathology, either directly or through downstream effects such as neuroinflammation.”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [24]
In the citing paper
“Initial histopathological studies investigating the relationship between amyloid plaques and apoE isoforms demonstrated a positive correlation between plaque density and apoE ε4 allele dose (Rebeck et al., 1993; Schmechel et al., 1993).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Rebeck et al., 1993
In the citing paper
“By immunostaining, these activated astrocytes express both the LDLR and LRP (data not shown), consistent with the previous observations summarized above that these are the two primary members of the LDLR family that are expressed by activated astrocytes (4 -7, 29 -31).”
From Apolipoprotein E Receptors Mediate the Effects of β-Amyloid on Astrocyte Cultures (2000) · cites this paper as [6]
In the citing paper
“neural cells express a variety of apoE receptors in the low density lipoprotein receptor (LDLR) family (4 -7).”
From Apolipoprotein E Receptors Mediate the Effects of β-Amyloid on Astrocyte Cultures (2000) · cites this paper as [6]
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Metadata
- Authors
- William Rebeck, G., Reiter, J. S., Strickland, D. K., & Hyman, B. T.
- Affiliations
- Massachusetts General Hospital (US)
- American Red Cross (US)
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1993-10
- Volume
- 11
- Issue
- 4
- Pages
- 575-580
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2091924214
- Cited by
- 1,107
- References
- 8
- Citations by year
- 2026: 16 · 2025: 14 · 2024: 27 · 2023: 24 · 2022: 25 · 2021: 20 · 2020: 25 · 2019: 16 · 2018: 18 · 2017: 34 · 2016: 25 · 2015: 25 · 2014: 31 · 2013: 24 · 2012: 27
- FWCI
- 47.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01gm042581-09, 1f32ag005598-01)
- National Institute on Aging (AG-08487, AG05598)
- National Institute of General Medical Sciences (GM-42581)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, Alzheimer's disease, APOE ε4, amyloid plaques, apoE receptors, LDL receptor, LDL receptor-related protein, astrocytes
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Genotype, Hippocampus, Humans, Immunohistochemistry, Middle Aged, Receptors, Immunologic, Receptors, LDL, Reference Values, Temporal Lobe, Genetic Variation, Low Density Lipoprotein Receptor-Related Protein-1
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