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Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
Open accessAbstract
Apolipoprotein E (apoE) alleles determine the age-adjusted relative risk (ɛ4 > ɛ3) for Alzheimer's disease (AD). ApoE may affect AD pathogenesis by promoting deposition of the amyloid-β (Aβ) peptide and its conversion to a fibrillar form. To determine the effect of apoE on Aβ deposition and AD pathology, we compared APP V717F transgenic (TG) mice expressing mouse, human, or no apoE (apoE −/− ). A severe, plaque-associated neuritic dystrophy developed in APP V717F TG mice expressing mouse or human apoE. Though significant levels of Aβ deposition also occurred in APP V717F TG, apoE −/− mice, neuritic degeneration was virtually absent. Expression of apoE3 and apoE4 in APP V717F TG, apoE −/− mice resulted in fibrillar Aβ deposits and neuritic plaques by 15 months of age and substantially (>10-fold) more fibrillar deposits were observed in apoE4-expressing APP V717F TG mice. Our data demonstrate a critical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD.
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“To date, substantial evidence has demonstrated ApoE affects amyloid-β deposition in a dosage and isoform-specific fashion (ApoE4>ApoE3>ApoE2)96–100”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [98]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“APOE exerts toxic effects on the cerebrovascular system (694) and neurons (383, 384) and influences A 𝛃 clearance (60, 64, 98, 135, 256, 266, 278, 294, 315, 693), amyloid deposition (39, 256, 258, 266, 278, 314, 518, 612), and tau-related neurodegeneration (533) in an allele-dependent manner APOE4 > APOE3 > APOE2 .”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [256]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we and others have reported human apoE isoform-dependent differences in amyloid plaque deposition in APP-transgenic mice (E4 > E3 > E2) (10-14).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [10]
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“It has been previously demonstrated that co-deposition of apoE in Aβ plaques is a prerequisite for the occurrence of focal neuritic dystrophy [22,29].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“It has also been recognized that co-deposition of apoE in Aβ plaques promotes focal neurodegeneration in humans and in AD Tg mice [22,29,35].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [29]
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“Our findings remain consistent with the effects of apoE knock-out noted in several AD Tg mouse models, where lack of apoE was associated with absence of fibrillar Aβ deposits and prevented neurodegeneration [13,29,31,32].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Apoe knockout mice exhibit markedly reduced amyloid deposition and develop diffuse, amorphous plaques. [44–46].”
From Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice (2026) · cites this paper as [45]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Most AD patients have sporadic late-onset AD (LOAD), in which the apolipoprotein E (APOE) gene contains a predominant risk variant6,7.”
From APOE3 - R136S mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“ApoE strongly regulates brain amyloid-β (Aβ) deposition in a dose- and isoform-dependent manner (E4>E3>E2) (Bales et al., 1997; Holtzman et al., 2000; Schmechel et al., 1993).”
From Overexpressing low‐density lipoprotein receptor reduces tau‐associated neurodegeneration in relation to apoE‐linked mechanisms (2021) · cites this paper as Holtzman et al., 2000
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“Restoration of APOE expression in astrocytes alone is sufficient to induce formation of fibrillar plaques and microglia reactivity, extending findings from previous studies (Holtzman et al, 2000a; Liu et al, 2017b; Mahan et al, 2022).”
From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Holtzman et al, 2000a
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“The expression of human apoE isoform transgenes in PDAPP mice resulted in a marked delay in the deposition of Aβ and formation of neuritic plaques, compared to PDAPP mice expressing murine apoE or no apoE (Fagan et al., 2002; Holtzman et al., 2000; Holtzman et al., 1999).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Holtzman et al., 2000
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Initial studies using the PDAPP and Tg2576 APP transgenic mouse models that develop Aβ deposition demonstrated that the lack of murine apoE resulted in a significant decrease in Aβ deposition, along with an almost complete lack of true amyloid plaques and neuritic dystrophy (Bales et al., 1997; Holtzman et al., 2000; Holtzman et al., 1999).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Holtzman et al., 2000
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“APOE-TR mice exhibit APOE genotype-dependent effects on Aβ seeding, Aβ clearance and tau-dependent neurodegeneration when crossed with APP or MAPT mutant mice (Holtzman et al., 2000; Shi et al., 2017).”
From Cholesterol and matrisome pathways dysregulated in astrocytes and microglia (2022) · cites this paper as Holtzman et al., 2000
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In the citing paper
“Introduction of human APOE to existing FAD-Tg mice significantly delays plaque deposition, although once detected, plaque levels are generally greater with APOE4 than APOE3 (3, 6 -8).”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [7]
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In the citing paper
“APOE isoform-dependent amyloid deposition has been consistently observed in humans and Aβ depositing mouse models (Holtzman et al., 2000; Bales et al., 2009; Reiman et al., 2009; Morris et al., 2010).”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Holtzman et al., 2000
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In the citing paper
“APOE has been shown to influence Aβ plaque morphology.”
From Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice (2026) · cites this paper as [45]
The cited source says what the claim attributes to it.
In the citing paper
“Interestingly, the human apoE transgenic mice display an isoform-specific pattern of Aβ deposition in the hippocampus, with apoE4 mice having increased levels of Aβ deposits and more thioflavine-S positive plaques than apoE3 mice (Fagan et al., 2002; Holtzman et al., 2000).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Holtzman et al., 2000
The cited source says what the claim attributes to it.
In the citing paper
“Clearly, human apoE isoforms affect A metabolism and deposition differently than murine apoE, but whether this is due to altered clearance and/or structure of A in vivo remains to be determined.”
The cited source says what the claim attributes to it.
In the citing paper
“Data from transgenic mouse models produced more conflicting results with impaired plaque deposition seen in mice lacking murine APOE (Bales et al., 1997; Holtzman et al., 2000), but also in animals overexpressing the human APOE3 or APOE4 isoforms (Holtzman et al., 1999).”
From The Pro-Neurotrophin Receptor Sortilin Is a Major Neuronal Apolipoprotein E Receptor for Catabolism of Amyloid-β Peptide in the Brain (2013) · cites this paper as Holtzman et al., 2000
In the citing paper
“ApoE assists in Aβ clearance in an isoform-dependent manner wherein apoE2 > apoE3 > apoE4 [29, 30, 59].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [30]
In the citing paper
“Compared with other ApoE isoforms, ApoE4 exacerbates the deposition of amyloid plaques in the brain98–100.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [98]
In the citing paper
“Expression of mouse ApoE resulted in greater plaque formation than expression of human ApoE, and mouse ApoE preferentially promoted the formation of parenchymal plaques, while human ApoE promoted the formation of CAA [59, 60, 94].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [59]
In the citing paper
“This is further complicated by the fact that expression of different isoforms of human ApoE in transgenic mice results in different levels of plaque and CAA burden with apoE4 expression enhancing amyloid deposition compared to apoE3 or apoE2 [3, 21, 40, 59, 86, 178].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [59]
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Self-citation
Metadata
- Authors
- Holtzman, D. M., Bales, K. R., Tenkova, T., Fagan, A. M., Parsadanian, M., Sartorius, L. J., Mackey, B., Olney, J., McKeel, D., Wozniak, D., & Paul, S. M.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2000-02-29
- Volume
- 97
- Issue
- 6
- Pages
- 2892-2897
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC16026
- OpenAlex
- W2119556701
- Cited by
- 937
- References
- 31
- Citations by year
- 2026: 17 · 2025: 27 · 2024: 41 · 2023: 22 · 2022: 29 · 2021: 21 · 2020: 39 · 2019: 31 · 2018: 14 · 2017: 31 · 2016: 35 · 2015: 27 · 2014: 34 · 2013: 29 · 2012: 39
- FWCI
- 32.12
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association (AG13956)
- American Federation for Aging Research
- Ruth K. Broad Biomedical Research Foundation
- National Institutes of Health (AG13956)
- National Institute on Aging (R01AG013956, R37AG013956, AG13956)
- 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, amyloid-beta deposition, fibrillar amyloid-beta, neuritic plaques, neuritic dystrophy, APOE isoforms, APOE ε4, APOE3, amyloid plaques, mouse model
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Disease Models, Animal, Hippocampus, Humans, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, Nerve Degeneration, Thiazoles, Time Factors, Neurites, Genetic Predisposition to Disease, Protein Isoforms, Mice, Benzothiazoles, Plaque, Amyloid
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