Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition

Bales, Kelly R.; Verina, Tatyana; Dodel, Richard C.; Du, Yansheng; Altstiel, Larry; Bender, Mark; Hyslop, Paul; Johnstone, Edward M.; Little, Sheila P.; Cummins, David J.; Piccardo, Pedro; Ghetti, Bernardino; Paul, Steven M.

doi:10.1038/ng1197-263

Cited by 830Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition

Bales, Kelly R., Verina, Tatyana, Dodel, Richard C., Du, Yansheng, Altstiel, Larry, Bender, Mark, Hyslop, Paul, Johnstone, Edward M. +5 more·1997·Nature Genetics

DOI 10.1038/ng1197-263

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ApoE is strongly associated with the amount of fibrillar amyloid that deposits into plaques.
“ApoE is strongly associated with the amount of fibrillar amyloid that deposits into plaques (28).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [28]
The amount of apoE plays a role in determining the extent of Aβ accumulation in the brain.
“In addition to isoform status, it appears that the amount of apoE also plays a role in determining the extent of Aβ accumulation in the brain.”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Bales et al., 1997
Deletion of the endogenous murine Apoe gene causes a dramatic decrease in fibrillar and total Aβ deposition in APP transgenic mouse models.
“Initial studies clearly indicated that the deletion of the endogenous murine Apoe gene causes a dramatic decrease in fibrillar and total Aβ deposition in APP transgenic mouse models (Bales et al., 1997).”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Bales et al., 1997
Lack of apoE led to a dramatic decrease of amyloid deposition in APP transgenic mouse models.
“Previous studies demonstrated that the lack of apoE led to a dramatic decrease of amyloid deposition in APP transgenic mouse models (Bales et al., 1997; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997
Absence of apoE leads to a dramatic decrease in the levels of fibrillar Aβ deposits in APP transgenic mouse models.
“Previous studies demonstrated that the absence of apoE leads to a dramatic decrease in the levels of fibrillar Aβ deposits in APP transgenic mouse models (Bales et al., 1999; Bales et al., 1997; Holtzman et al., 2000a; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997

Lack of apoE leads to a dramatic reduction of fibrillar Aβ deposition in APP transgenic mouse models.
“Later, in vivo studies demonstrated that the lack of apoE led to a dramatic reduction of fibrillar Aβ deposition in APP transgenic mouse models (Bales et al., 1999; Bales et al., 1997; Holtzman et al., 2000a; Holtzman et al., 2000b).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Bales et al., 1997
Reducing ApoE in mouse models of amyloidosis greatly reduces plaque formation.
“Reducing ApoE in mouse models of amyloidosis greatly reduces plaque formation (7, 8, 33, 34).”
From The E3 ubiquitin ligase Idol controls brain LDL receptor expression, ApoE clearance, and Aβ amyloidosis (2015) · cites this paper as [33]
Genetic deletion and pharmacological reduction of APOE reduce Aβ deposition in mouse models of Alzheimer's disease.
“Both genetic deletion and pharmacological reduction of APOE reduced Aβ deposition in mouse models of AD. 3 , 4 , 5 , 6 , 7 , 8 , 9”
From Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors (2025) · cites this paper as [3]
Deletion of Apoe reduces amyloid deposition in transgenic mouse models of AD.
“Notably, deletion of Apoe reduces amyloid deposition in transgenic mouse models of AD. 3 , 4”
From Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors (2025) · cites this paper as [3]
In several AD Tg mouse models, lack of apoE is associated with absence of fibrillar Aβ deposits and prevented neurodegeneration.
“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 [31]
Independent of apoE isoform, the amount of apoE in the brain appears to be critical for determining the extent of amyloid deposition.
“Independent of apoE isoform, the amount of apoE in the brain appears to be critical for determining the extent of amyloid deposition [25,26].”
From Measurement of apolipoprotein E and amyloid β clearance rates in the mouse brain using bolus stable isotope labeling (2012) · cites this paper as [25]
ApoE gene deletion in APP transgenic mice leads to dramatically decreased amyloid plaques without affecting Aβ production.
“ApoE gene deletion in APP transgenic mice leads to dramatically decreased amyloid plaques without affecting Aβ production (Bales et al., 1997).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Bales et al., 1997
ApoE gene knockout in AD transgenic mice is associated with marked reduction in Aβ plaque and CAA deposits.
“The pivotal role of ApoE in brain Ab accumulation was confirmed by showing a marked reduction in Ab plaque and CAA deposits associated with the Apoe gene knockout (KO) in AD transgenic (Tg) mice.14”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [14]
Similar effects of ApoE KO were previously reported in APP V717F and APP SW lines, representing more latent models of Aβ pathology in which thioflavin-S detects the first plaques around the age of 1 year.
“Similar effects of the ApoE KO were previously reported in APP V717F and APP SW lines, representing more latent models of Ab pathology in which thioflavin-S detects the first plaques around the age of 1 year.14,55”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [14]
Reducing ApoE levels is generally protective in AD models.
“Reducing ApoE levels is generally protective in AD models1,4–6.”
From Decreased lipidated ApoE‐receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes (2025) · cites this paper as [4]
ApoE is co-deposited in senile plaques and plays a crucial role in fibrillar plaque formation.
“Previous studies showed that apoE is co-deposited in senile plaques and plays a crucial role in fibrillar plaque formation (23, 24).”
From APOE3 -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [23]
In amyloid precursor protein-expressing transgenic mice, deletion of the mouse apoE gene inhibits development of fibrillar amyloid plaques.
“In amyloid precursor proteineexpressing transgenic mice, deletion of mouse apoE gene inhibits development of fibrillar amyloid plaques [80,81].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [80]
ApoE regulates brain amyloid-β deposition in a dose- and isoform-dependent manner (E4>E3>E2).
“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 Bales et al., 1997
APP transgenic mice lacking endogenous mouse apoE display a significant decrease of amyloid pathology.
“APP transgenic mice lacking endogenous mouse apoE display a significant decrease of amyloid pathology”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Bales et al 1997
ApoE-deficient APP transgenic mice display virtually no fibrillar Aβ deposits nor neuritic degeneration.
“apoE-deficient APP transgenic mice display virtually no fibrillar Aβ deposits nor neuritic degeneration”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Bales et al 1997
Initial studies using PDAPP and Tg2576 APP transgenic mouse models 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.
“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 Bales et al., 1997
APOE, the strongest genetic risk factor for LOAD, largely increases risk by influencing Aβ seeding and clearance.
“In addition, the strongest genetic risk factor for LOAD, apolipoprotein E, APOE, in large part appears to increase risk via influencing Aβ seeding and clearance”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Bales et al., 1997
ApoE affects amyloid-β deposition in a dosage and isoform-specific fashion (ApoE4>ApoE3>ApoE2).
“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 [96]
Transgenic mouse studies confirmed that ApoE was necessary for the formation of fibrillar amyloid plaques and CAA.
“Transgenic mouse studies confirmed that ApoE was necessary for the formation of fibrillar amyloid plaques and CAA [4, 5, 41, 61], however they also identified important differences between mouse and human ApoE.”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [5]

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Self-citation

Authors: Bales, K. R., Verina, T., Dodel, R. C., Du, Y., Altstiel, L., Bender, M., Hyslop, P., Johnstone, E. M., Little, S. P., Cummins, D. J., Piccardo, P., Ghetti, B., & Paul, S. M.
Affiliations: Eli Lilly (United States) (US)
Indiana University School of Medicine (US)
Philipps University of Marburg (DE)
ORCID: Dodel, Richard C.
Du, Yansheng
Bender, Mark
Hyslop, Paul
Ghetti, Bernardino
Paul, Steven M.
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 1997-11
Volume: 17
Issue: 3
Pages: 263-264
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/ng1197-263
OpenAlex: W1981554609
Cited by: 830
References: 14
Citations by year: 2026: 11 · 2025: 8 · 2024: 27 · 2023: 18 · 2022: 25 · 2021: 19 · 2020: 27 · 2019: 24 · 2018: 16 · 2017: 21 · 2016: 20 · 2015: 19 · 2014: 21 · 2013: 16 · 2012: 20
FWCI: 26.51
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Genetics (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, amyloid deposition, Alzheimer's disease, APOE genotype, apolipoprotein E deficiency
MeSH terms: Age Factors, Alzheimer Disease, Animals, Apolipoproteins E, Brain, Humans, Immunohistochemistry, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, RNA, Messenger, Polymerase Chain Reaction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice, Knockout, Mice

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Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition

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